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Abstract Introduction In response to the COVID-19 crisis, this study aimed to introduce a new virtual teaching model for anatomy education that combines Peer-Assisted Learning (PAL) and flipped classrooms, aligning with constructivist principles. Method The Flipped Peer Assisted (FPA) method was implemented in a virtual neuroanatomy course for second-year medical students at Birjand University of Medical Sciences via a descriptive study. The method involved small groups of PAL, with peer learning serving as educational assistants and the teacher acting as a facilitator. Educational content was uploaded to the university’s learning management system (LMS). The opinion of medical students regarding the teaching method were evaluated using a 15-item questionnaire on a five-point Likert scale. Results A total of 210 students participated in the instruction using the FPA method. The analysis of students’ scores revealed an average score of 26.75 ± 3.67 on the 30-point test. According to student feedback, this teaching method effectively motivated students to study, enhanced teamwork and communication skills, transformed their perspective on the anatomy course, provided opportunities for formative assessment and feedback, and demonstrated the teacher’s dedication to education. Conclusion The FPA model demonstrates its effectiveness in transforming traditional classroom teaching and fostering teaching and learning in virtual environments, particularly during pandemics like COVID-19. This model holds promise for enhancing anatomy education in challenging circumstances.

Malathion, a widely used organophosphate, is known for its relatively low toxicity and extensive application. However, it has been found to act as a female reproductive toxicant by causing oxidative stress, apoptosis, autophagy, and hormonal imbalances. Hesperidin, a flavonoid belonging to the flavanone class, exhibits various beneficial properties such as antioxidant and anti-inflammatory effects, which can potentially counteract harmful effects. The objective of this study was to examine how hesperidin and malathion impact the expression of miRNAs and genes linked to apoptosis and inflammation. Balb/c mice (n = 40) were divided into four groups: hesperidin (20 mg/kg), malathion (3 mg/kg), hesperidin+malathion, and control. After a 35-day intraperitoneal treatment, the mice were sacrificed. The left ovaries were used for analyzing the expression of miRNA-146a-5p, miRNA-129-3p, miRNA-96-5p, NF-κB, Bax, and Bcl-2 through RT-qPCR, as well as the levels of several cytokines using the ELISA method. The right ovaries were examined through histological and immunohistochemical techniques using H&E and NF-κB staining. Malathion exposure led to an increased Bax/Bcl-2 ratio, upregulated expression of Bax and NF-κB, elevated levels of IFN-γ, IL-2, and IL-6, enhanced expression of miRNA-146a-5p, decreased expression of miRNA-129-3p and miRNA-96-5p, and reduced levels of IL-4 and IL-10. Additionally, malathion-exposed ovaries exhibited structural abnormalities and disrupted architecture, accompanied by heightened NF-κB immunoreactivity. Conversely, treatment with hesperidin showed its capacity to counteract the detrimental consequences of malathion on the ovaries by alleviating or reversing these changes. In conclusion, hesperidin showed protective effects against malathion-induced ovarian toxicity by modulating cytokine production, apoptosis, inflammation, and miRNA expression.

Toxic agents are broadly present in the environment, households, and workplaces. Contamination of food and drinking water with these agents results in entry of these materials to the body. The crosstalk between these agents and microRNAs (miRNAs) affects pathoetiology of several disorders. These agents can influence the redox status, release of inflammatory cytokines and mitochondrial function. Altered expression of miRNA is involved in the dysregulation of several pathophysiological conditions and signaling pathways. These molecules are also implicated in the adaption to environmental stimuli. Thus, the interactions between miRNAs and toxic materials might participate in the hazardous effects of these materials in the body. This review describes the effects of the toxic materials on miRNAs and the consequences of these interactions on the human health.

Exosomes are an important group of extracellular vesicles that transfer several kinds of biomolecules and facilitate cell-cell communication. The content of exosomes, particularly the amounts of microRNA (miRNAs) inside these vesicles, demonstrates a disease-specific pattern reflecting pathogenic processes and may be employed as a diagnostic and prognostic marker. miRNAs may enter recipient cells through exosomes and generate a RISC complex that can cause degradation of the target mRNAs or block translation of their corresponding proteins. Therefore, exosome-derived miRNAs constitute an important mechanism of gene regulation in recipient cells. The miRNA content of exosomes can be used as an important tool in the detection of diverse disorders, particularly cancers. This research field has an important situation in cancer diagnosis. In addition, exosomal microRNAs offer a great deal of promise in the treatment of human disorders. However, there are still certain challenges to be resolved. The most important challenges are as follow: the detection of exosomal miRNAs should be standardized, exosomal miRNAs-associated studies should be conducted in large number of clinical samples, and experiment settings and detection criteria should be consistent across different labs. The goal of this article is to present an overview of the effects of exosome-derived microRNAs on a variety of diseases, including gastrointestinal, pulmonary, neurological, and cardiovascular diseases, with a particular emphasis on malignancies.

Abstract Background: Ovarian tissue extract (OTE) and sodium selenite (SS) enhance the growth and maturation of preantral follicles in a dose-dependent manner. Objective: The present study was designed to bring more information regarding the mechanism of OTE and SS on the mRNA expression of follicle-stimulating hormone receptors (FSHR) and the proliferation cell nuclear antigens (PCNA) of in vitro matured isolated follicles. Materials and Methods: The tissue extract was prepared from adult ovaries. The preantral follicles (n = 266) were isolated from 12-16-day-old mice and cultured in the control, experimental I (10 ng/ml SS), and experimental II (OTE) groups for 12 days. The follicular diameter, survival, and maturation rates, also, the production of 17-β-estradiol and progesterone, and the follicular expression of PCNA and FSH receptor genes were analyzed. Results: The survival rate of follicles in the SS-treated group (84.58%) was significantly higher than that OTE (75.63%; p = 0.023) and control (69.38%; p = 0.032) groups. The mean diameter of culture follicles in experimental group I (403.8 μm) and experimental group II (383.97 μm) increased significantly in comparison with the control group (342.05 μm; p = 0.032). The developmental rate of follicles, percentages of antrum formation, released metaphase II oocytes (p = 0.027; p = 0.019 respectively), production of hormones and the expression of 2 studied genes were significantly increased in both experimental groups in compare with control group (p = 0.021; p = 0.023 respectively). Conclusion: The OTE and SS have a positive effect on development of mouse preantral follicles via over-expression of FSHR and PCNA genes.

Objective: Malathion (MAL), a pesticide used for decades, is a highly toxic substance. Several studies have documented the negative effects of such agents on reproductive organ physiology, but the precise mechanism of action in the induction of ovarian dysfunction remains unclear. Therefore, the purpose of this research was to examine the effects of the antioxidant hesperidin (HES) on ovarian damage and toxicity caused by malathion. Materials and methods: In this experiment, forty adult female bulb/c mice weighing 27–30 g were categorized into four groups, namely hesperidin (20 mg/kg, i.p.), malathion (3 mg/kg, i.p.), malathion + hesperidin, and control groups. Following a period of 35 consecutive days of treatment, mice were euthanized, and their ovarian tissues were gathered for the purposes of histopathological analysis by H&E staining, immunohistochemical assessment via proliferating cell nuclear antigen (PCNA) and follicle-stimulating hormone receptor (FSHR) immunostaining, and biochemical evaluation via measuring the levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β). In addition, serum samples were collected from the blood of mice to perform hormonal analyses, especially 17β-estradiol (E2), progesterone (P4), luteinizing hormone (LH), and follicle-stimulating hormone (FSH). Results: The results demonstrated that MAL exposure resulted in the development of abnormalities in the architecture and structure of ovaries. Also, the treatment of mice with MAL led to declined follicular counts at all three stages, namely, primary, secondary, and tertiary, reduced serum levels of sex hormones, decreased immunoreactivity of FSHR and PCNA, and diminished activity of CAT and SOD enzymes. In contrast, it caused an increase in MDA, IL-1β, and TNF-α, as well as the count of atretic follicles. Nonetheless, it was observed that HES exhibited the ability to ameliorate the deleterious impacts of malathion across all the aforementioned parameters. Conclusion: Treatment with HES via upregulating the protein expression of PCNA and FSHR and activating antioxidant defense was able to ameliorate the adverse effects of MAL on ovarian tissues.

Natural killer cells (NK cells) are a type of cytotoxic lymphocytes which are involved in innate immunity, alongside with assisting with adaptive immune response. Since they have cytotoxic effects, disruptions in their functionality and development leads to a variety of conditions, whether malignant or non-malignant. The profile and interaction of these non-coding RNAs and NK cells in different conditions is extensively studied, and it is now approved that if dysregulated, non-coding RNAs have detrimental effects on NK cell activity and can contribute to the pathogenesis of diverse disorders. In this review, we aim at a thorough inspection on the role of different non-coding RNAs on the activity and development of NK cells, in a broad spectrum of conditions, including blood-related disorders, viral infections, neurological diseases, gastrointestinal disorders, lung disorders, reproductive system conditions and other types of maladies, alongside with providing insight to the future non-coding RNA-NK cell studies.

Abstract Resveratrol (3,5,4′-trihydroxy-trans-stilbene) is a natural phenol that is present in the skin of the grape, blueberry, raspberry, mulberry, and peanut. This substance is synthesized in these plants following injury or exposure to pathogens. Resveratrol is used as a dietary supplement for a long time and its effects have been assessed in animal models of human disorders. It has potential beneficial effects in diverse pathological conditions such as diabetes mellitus, obesity, hypertension, neoplastic conditions, Alzheimer's disease, and cardiovascular disorders. Notably, resveratrol has been found to affect the expression of several genes including cytokine coding genes, caspases, matrix metalloproteinases, adhesion molecules, and growth factors. Moreover, it can modulate the activity of several signaling pathways such as PI3K/AKT, Wnt, NF-κB, and Notch pathways. In the current review, we summarize the results of studies that reported modulatory effects of resveratrol on the expression of genes and the activity of signaling pathways. We explain these results in two distinct sections of non-neoplastic and neoplastic conditions.

SIRT1 is a member of the sirtuin family functioning in the process of removal of acetyl groups from different proteins. This protein has several biological functions and is involved in the pathogenesis of metabolic diseases, malignancy, aging, neurodegenerative disorders and inflammation. Several long non-coding RNAs (lncRNAs), microRNAs (miRNAs) and circular RNAs (circRNAs) have been found to interact with SIRT1. These interactions have been assessed in the contexts of sepsis, cardiomyopathy, heart failure, non-alcoholic fatty liver disease, chronic hepatitis, cardiac fibrosis, myocardial ischemia/reperfusion injury, diabetes, ischemic stroke, immune-related disorders and cancers. Notably, SIRT1-interacting non-coding RNAs have been found to interact with each other. Several circRNA/miRNA and lncRNA/miRNA pairs that interact with SIRT1 have been identified. These axes are potential targets for design of novel therapies for different disorders. In the current review, we summarize the interactions between three classes of non-coding RNAs and SIRT1.

Endocrine disruptors such as bisphenol A (BPA) and some of its analogues, including BPS, BPAF, and BPE, are used extensively in the manufacture of plastics. These synthetic chemicals could seriously alter the functionality of the female reproductive system. Although the number of studies conducted on other types of bisphenols is smaller than the number of studies on BPA, the purpose of this review study was to evaluate the effects of bisphenol compounds, particularly BPA, on hormone production and on genes involved in ovarian steroidogenesis in both in vitro (human and animal cell lines) and in vivo (animal models) studies.The current data show that exposure to bisphenol compounds has adverse effects on ovarian steroidogenesis. For example, BPA, BPS, and BPAF can alter the normal function of the hypothalamic-pituitary-gonadal (HPG) axis by targeting kisspeptin neurons involved in steroid feedback signals to gonadotropin-releasing hormone (GnRH) cells, resulting in abnormal production of LH and FSH. Exposure to BPA, BPS, BPF, and BPB had adverse effects on the release of some hormones, namely 17-β-estradiol (E2), progesterone (P4), and testosterone (T). BPA, BPE, BPS, BPF, and BPAF are also capable of negatively altering the transcription of a number of genes involved in ovarian steroidogenesis, such as the steroidogenic acute regulatory protein (StAR, involved in the transfer of cholesterol from the outer to the inner mitochondrial membrane, where the steroidogenesis process begins), cytochrome P450 family 17 subfamily A member 1 (Cyp17a1, which is involved in the biosynthesis of androgens such as testosterone), 3 beta-hydroxysteroid dehydrogenase enzyme (3β-HSD, involved in the biosynthesis of P4), and cytochrome P450 family 19 subfamily A member 1 (Cyp19a1, involved in the biosynthesis of E2). Exposure to BPA, BPB, BPF, and BPS at prenatal or prepubertal stages could decrease the number of antral follicles by activating apoptosis and autophagy pathways, resulting in decreased production of E2 and P4 by granulosa cells (GCs) and theca cells (TCs), respectively. BPA and BPS impair ovarian steroidogenesis by reducing the function of some important cell receptors such as estrogens (ERs, including ERα and ERβ), progesterone (PgR), the orphan estrogen receptor gamma (ERRγ), the androgen receptor (AR), the G protein-coupled estrogen receptor (GPER), the FSHR (follicle-stimulating hormone receptor), and the LHCGR (luteinizing hormone/choriogonadotropin receptor). In animal models, the effects of bisphenol compounds depend on the type of animals, their age, and the duration and dose of bisphenols, while in cell line studies the duration and doses of bisphenols are the matter.

Programmed death-ligand 1 (PD-L1) is a transmembrane protein with essential roles in the suppression of adaptive immune responses. As an immune checkpoint molecule, PD-L1 can be exploited by cancer cells to evade the anti-tumor attacks initiated by the immune system. Thus, blockade of the PD1/PD-L1 axis can eliminate the suppressive signals and release the antitumor immune responses. Identification of the underlying mechanisms of modulation of the activity of the PD1/PD-L1 axis would facilitate the design of more efficacious therapeutic options and better assignment of patients for each option. Recent studies have confirmed the interactions between miRNAs/lncRNAs/circ-RNAs and the PD1/PD-L1 axis. In the current review, we give a summary of interactions between these transcripts and PD-L1 in the context of cancer. We also overview the consequences of these interactions in the determination of the response of patients to anti-cancer drugs.

Background: Testicular tissues could damage by ionizing radiation (IR) during the treatment of pelvic cancers. The aim of this study was to investigate both the protective and therapeutic effects of chlorogenic acid (CGA) on IR-induced mouse testis tissue damage. Methods: In this experimental study, 70 mice were divided into 3 groups, including group 1 (normal saline), group 2 (IR + normal saline), and group 3 (IR + 5, 10, 20, 40, and 80 mg/kg) CGA via I.P injection. Animals in groups 2 and 3 received a dose of 2.0 Gy total-body irradiation in a single fraction. At two determined time points (16 h and 35 days after exposure), the testis and caudal part of both epididymis were isolated and underwent subsequent analyses. Results: The results showed that irradiation of mice caused massive damage to spermatogenesis, seminiferous tubules, basal lamina, Leydig cells, and sperm parameters. Further biochemical assessment of the data demonstrated that 40 mg/kg CGA almost restored MDA to a normal level. In addition, the level of SOD, TAC, and GSH were significantly increased in the 40 mg/kg CGA treated group. Molecular evidence confirmed the protective effects of CGA and also revealed that the ratio of Bax/Bcl-2 in the presence of 40 mg/kg CGA was significantly decreased compared to IR and some treated groups. Conclusion: The protective and therapeutic effects of CGA on testis were found to be positively correlated with the dose level.

NLR family pyrin domain containing 3 (NLRP3) is expressed in immune cells, especially in dendritic cells and macrophages and acts as a constituent of the inflammasome. This protein acts as a pattern recognition receptor identifying pathogen-associated molecular patterns. In addition to recognition of pathogen-associated molecular patterns, it recognizes damage-associated molecular patterns. Triggering of NLRP3 inflammasome by molecules ATP released from injured cells results in the activation of the inflammatory cytokines IL-1β and IL-18. Abnormal activation of NLRP3 inflammasome has been demonstrated to stimulate inflammatory or metabolic diseases. Thus, NLRP3 is regarded as a proper target for decreasing activity of NLRP3 inflammasome. Recent studies have also shown abnormal activity of NLRP3 in ischemia/reperfusion (I/R) injuries. In the current review, we have focused on the role of this protein in I/R injuries in the gastrointestinal, neurovascular and cardiovascular systems.

Rho Associated Coiled-Coil Containing Protein Kinase 1 (ROCK1) is a protein serine/threonine kinase which is activated upon binding with the GTP-bound form of Rho. This protein can modulate actin-myosin contraction and stability. Moreover, it has a crucial role in the regulation of cell polarity. Therefore, it participates in modulation of cell morphology, regulation of expression of genes, cell proliferation and differentiation, apoptotic processes as well as oncogenic processes. Recent studies have highlighted interactions between ROCK1 and several non-coding RNAs, namely microRNAs, circular RNAs and long non-coding RNAs. Such interactions can be a target of medications. In fact, it seems that the interactions are implicated in therapeutic response to several medications. In the current review, we aimed to explain the impact of these interactions in the pathoetiology of cancers as well as non-malignant disorders.

Calcium binding proteins (CBP) are a group of proteins mediating the effects of calcium on cellular functions. These proteins can regulate calcium levels inside the cells and contribute in several cellular functions through transporting this ion across cell membranes or decoding related signals. Recent studies have shown that several non-coding RNAs interact with CBPs to affect their expression or activity. The interactions between these transcripts and CBPs have implications in the pathoetiology of human disorders, including both neoplastic and non-neoplastic conditions. In the current review, we describe the interactions between three classes of non-coding RNAs (long non-coding RNAs, circular RNAs, and microRNAs) and a number of CBPs, particularly CAB39, S100A1, S100A4, S100A7 and S100P. This kind of interaction has been verified in different pathological contexts such as drug-induced cardiotoxicity, osteoblasts cytotoxicity, acute lung injury, myocardial ischemia/reperfusion injury, proliferative diabetic retinopathy, glomerulonephritis, as well as a wide array of neoplastic conditions.

Programmed cell death (PDCD) family of proteins includes at least 12 members, function of seven of them being more investigated. These members are PDCD1, PDCD2, PDCD4, PDCD5, PDCD6, PDCD7 and PDCD10. Consistent with the important roles of these proteins in the regulation of apoptosis, dysregulation of PDCDs is associated with diverse disorders ranging from intervertebral disc degeneration, amyotrophic lateral sclerosis, immune thrombocytopenia, type 1 diabetes, congenital hypothyroidism, Alzheimer’s disease to different types of cancers. More recently, the interaction between non-coding RNAs and different members of PDCD family is being discovered. In the current study, we described the functional interactions between PDCDs and two classes of non-coding RNAs, namely microRNAs (miRNAs) and long non-coding RNAs (lncRNAs). miR-21 and miR-183 are two miRNAs whose interactions with PDCDs have been assessed in different contexts. The lncRNAs interaction with PDCDs is mainly assessed in the context of neoplasia indicating the role of MALAT1, MEG3, SNHG14 and LINC00473 in this process.

Ectopic pregnancy (EP) is reported in about 1%–2% of pregnant females and is associated with mortality and morbidity. Several genetic and environmental factors might modulate occurrence of EP. Prediction of EP and patients' follow-up is an important task in management of pregnancy. MicroRNAs (miRNAs) as non-coding RNAs with sizes between 21 and 24 nucleotides have been shown to regulate several aspects of implantation and early fetal life. They have potential role in early detection of EP especially considering their presence in body fluids such as serum. Assessment of their expression in serum might provide a noninvasive method for diagnosis and patients' follow-up. However, data regarding their role in EP is not sufficient due to small sample sizes of the studies. Future studies are required to find miRNAs that regulate expression of EP-associated genes such as VEGFA, EGFR, ESR1 and immune response-related genes to provide new diagnostic biomarkers for EP.

Fibrosis is the endpoint of pathological remodeling. This process contributes to the pathogenesis of several chronic disorders and aging-associated organ damage. Different molecular cascades contribute to this process. TGF-β, WNT, and YAP/TAZ signaling pathways have prominent roles in this process. A number of long non-coding RNAs and microRNAs have been found to regulate organ fibrosis through modulation of the activity of related signaling pathways. miR-144-3p, miR-451, miR-200b, and miR-328 are among microRNAs that participate in the pathology of cardiac fibrosis. Meanwhile, miR-34a, miR-17-5p, miR-122, miR-146a, and miR-350 contribute to liver fibrosis in different situations. PVT1, MALAT1, GAS5, NRON, PFL, MIAT, HULC, ANRIL, and H19 are among long non-coding RNAs that participate in organ fibrosis. We review the impact of long non-coding RNAs and microRNAs in organ fibrosis and aging-related pathologies.

Breast cancer is the most frequently diagnosed cancer among females. Gene expression profiling methods have shown the deregulation of several genes in breast cancer samples and have confirmed the heterogeneous nature of breast cancer at the genomic level. microRNAs (miRNAs) are among the recently appreciated contributors in breast carcinogenic processes. These small-sized transcripts have been shown to partake in breast carcinogenesis through modulation of apoptosis, autophagy, and epithelial–mesenchymal transition. Moreover, they can confer resistance to chemotherapy. Based on the contribution of miRNAs in almost all fundamental aspects of breast carcinogenesis, therapeutic intervention with their expression might affect the course of this disorder. Moreover, the presence of miRNAs in the peripheral blood of patients potentiates these transcripts as tools for non-invasive diagnosis of breast cancer.

Non-coding RNAs have been found to regulate several developmental processes among them is osteogenesis. Although these transcripts have several distinct classes, two classes i.e. microRNAs and long non-coding RNAs have attained more attention. These transcripts regulate intramembranous as well as endochondral ossification processes. The effects of microRNAs on osteogenesis are mostly mediated through modulation of Wnt/β-catenin and TGFβ/BMP pathways. Long non-coding RNAs can directly affect expression of these pathways or osteogenic transcription factors. Moreover, they can serve as a molecular sponge for miRNAs. MALAT1/miR-30, MALAt1/miR-214, LEF1-AS1/miR-24-3p, MCF2L-AS1/miR-33a, MSC-AS1/miR-140-5p and KCNQ1OT1/miR-214 are examples of such kind of interaction between lncRNAs and miRNAs in the context of osteogenesis. In the current paper, we explain these two classes of non-coding RNAs in the osteogenesis and related disorders.

Residing on chromosome 20q13.13, Zinc Finger NFX1-Type Containing 1 (ZNFX1) antisense RNA 1 (ZFAS1) is a transcript which has been primarily recognized as a modulator of differentiation of alveolar and epithelial cell in the mammary gland. This long non-coding RNA (lncRNA) partakes in the molecular cascades leading to several non-neoplastic conditions such as osteoarthritis, epilepsy, rheumatoid arthritis, atherosclerosis, pulmonary fibrosis, myocardial infarction, and cardiac dysfunction. More importantly, ZFAS1 is considered as an oncogene in almost all types of cancers. Using expression amounts of ZFAS1, it is possible to forecast the clinical outcome of patients with different neoplasms such as colorectal cancer, gastric cancer, cholangiocarcinoma, hepatoblastoma, and other types of cancer. We describe the role of ZFAS1 in the development of neoplastic and non-neoplastic disorders.

Treatment of cancer in young adults is associated with several side effects, particularly in the reproductive system. Detrimental effects of chemotherapy on the germ cells depend on many factors including primary semen parameters, the way of drug administration, the kind and dose of chemotherapeutic regimens, and the phase of spermatogenesis during the time of drug administration. Lack of appropriate fertility preservation treatments particularly in the affected children necessitates the introduction of methods to amend the harmful effects of chemotherapeutic agents on male germ cells. Several studies have assessed the toxic effects of chemotherapeutic agents in rodent models and tested a number of antioxidants to evaluate their possible impact on the preservation of sperm cells. In the present manuscript, we describe the effects of the mostly investigated chemotherapeutic drugs in this regard i.e., cisplatin, doxorubicin, paclitaxel, 5-fluorouracil, and cyclophosphamide. As several in vivo and in vitro studies have shown the impact of antioxidants on chemotherapy-induced damage of sperms, we also describe the protective effects of antioxidants in this regard.

Self-renewal and differentiation into diverse cells are two main characteristics of stem cells. These cells have important roles in development and homeostasis of different tissues and are supposed to facilitate tissue regeneration. Function of stem cells is regulated by dynamic interactions between external signaling, epigenetic factors, and molecules that regulate expression of genes. Among the highly appreciated regulators of function of stem cells are long non-coding RNAs (lncRNAs) and microRNAs (miRNAs). Impact of miR-342-5p, miR-145, miR-1297, miR-204-5p, miR-132, miR-128-3p, hsa-miR-302, miR-26b-5p and miR-10a are among miRNAs that regulate function of stem cells. Among lncRNAs, AK141205, ANCR, MEG3, Pnky, H19, TINCR, HULC, EPB41L4A-AS1 and SNHG7 have important roles in the regulation of stem cells. In the current paper, we aimed at reviewing the importance of miRNAs and lncRNAs in differentiation of stem cells both in normal and diseased conditions. For this purpose, we searched PubMed/Medline and google scholar databases using “stem cell” AND “lncRNA”, or “long non-coding RNA”, or “microRNA” or “miRNA”.

Macrophage polarization is a process through which macrophages attain unique functional features as a response to certain stimuli from their niche. Lipopolysaccharide and Th1 cytokines induce generation of M1 macrophages. On the other hand, IL-4, IL-13, IL-10, IL-33, and TGF-β induce polarization of macrophages towards M2 phenotype. This process is also modulated by a number of miRNAs and lncRNAs. miR-375, miR-let7, miR-34a, miR-155, miR-124, miR-34a, miR-511-3p, miR-99a, miR-132 and miR-145-3p are among miRNAs that regulate macrophage polarization. Meanwhile, macrophage polarization is influenced by some lncRNAs such as H19, NRON, MEG3, GAS5, RN7SK, and AK085865. Macrophage polarization has functional significance in a wide range of human disorders particularly immune disorders and cancer. In addition, the effect of certain drugs in modulation of macrophage polarization is exerted through modulation of expression of non-coding RNAs. In the current manuscript, we provide a summary of studies aimed to identification of this aspect of non-coding RNAs.

Atrophy is defined as a reduction in cell, organ, or tissue size after reaching their normal mature sizes because of loss of organelles, cytoplasmic compartments, and proteins. This process is also involved in the pathogenesis of human disorders. Inadequate nourishment, poor circulation, inadequate hormonal support, defects in nerve supply of the tissue, disproportionate induction of apoptosis in the tissue, and absence of exercise are some underlying causes of atrophy. Recently, several non-coding RNAs (ncRNAs) have been identified that regulate atrophy, thus participating in the pathobiology of related disorders such as neurodegenerative/ neuromuscular diseases, age-related muscle atrophy, and cardiac tissue atrophy. In the current review, we have focused on two classes of ncRNAs namely long ncRNAs (lncRNAs) and microRNAs (miRNAs) to unravel their participation in atrophy-associated disorders.

Quercetin is a flavonoid existing in different herbs, fruits, seeds, nuts and tea. It has beneficial effects on human health through mediating antioxidant activities, immune-modulatory impacts and regulating metabolic pathways. These effects are most probably induced through modulation of activity of signaling pathways and expression of genes. Several in vitro studies have verified anti-proliferative effects of quercetin and its effect on expression of apoptotic genes and cell cycle-related genes. Moreover, through modulation of a number of proteins such as NF-kB, PARP, STAT3, Bax, Bcl-2, COX2, and cytokines, quercetin has beneficial effects in neurodegenerative disorders, liver diseases and diabetes. PI3K/AKT is the mostly linked pathway with beneficial effects of quercetin. In the current manuscript, we explain the impact of quercetin on expression of genes and function of cellular signaling cascades in different contexts.

Toll-like receptors (TLRs) are a large group of pattern recognition receptors which are involved in the regulation of innate immune responses. Based on the interplay between TLRs and adapter molecules, two distinctive signaling cascades, namely the MyD88-dependent and TRIF-dependent pathways have been recognized. TLRs are involved in the development of a wide variety of diseases including cancer and autoimmune disorders. A large body of evidence has shown interaction between two classes of non-coding RNAs, namely microRNAs (miRNAs) and long noncoding RNAs (lncRNAs). These interactions have prominent roles in the pathogenesis of several disorders including infectious disorders, autoimmune conditions and neoplastic disorders. This review aims at description of the interaction between these non-coding RNAs and TLRs.

miR-379 is a miRNA transcribed from the MIR379 locus on 14q32.31. This miRNA is located in an evolutionarily conserved miRNA cluster in an imprinted region that contains DLK1 and DIO3 genes. The mouse homolog of this miRNA has been shown to be under-expressed in response to glucocorticoid receptor deficiency. Moreover, miR-379 has a tumor-suppressive role in a wide variety of tissues including the brain, breast, lung, and liver. In addition to restraining cell proliferation and migration, miR-379 can suppress the epithelial-mesenchymal transition process. Abnormal expression of this miRNA implies the pathogenesis of Duchene muscular dystrophy, spinal cord injury, diabetic nephropathy, acute myocardial infarction, and premature ovarian failure. This review aims to the summarization of the role of miR-379 in neoplastic and non-neoplastic conditions.

Apoptosis is a coordinated cellular process that occurs in several physiological situations. Dysregulation of apoptosis has been documented in numerous pathological situations, particularly cancer. Non-coding RNAs regulate apoptosis via different mechanisms. Lung cancer is among neoplastic conditions in which the role of non-coding RNAs in the regulation of apoptosis has been investigated. Non-coding RNAs that regulate apoptosis in lung cancer have functional interactions with PI3K/Akt, PTEN, GSK-3β, NF-κB, Bcl-2, Bax, p53, mTOR and other important cancer-related pathways. Globally, over-expression of apoptosis-blocking non-coding RNAs has been associated with poor prognosis of patients, while apoptosis-promoting ones have the opposite effect. In the current paper, we describe the impact of lncRNAs and miRNAs on cell apoptosis in lung cancer.

Stem cells have two important features, namely the ability for self-renewal and the capacity to differentiate into some cell kinds with specialized functions. These two features are also present in cancer stem cells (CSCs). These cells have been detected in almost all kinds of cancers facilitating their tumorigenicity. Molecular cascades that control self-renewal of stem cells, namely the Wnt, Notch, and Hedgehog pathways have been suggested to influence CSCs functions as well. Moreover, non-coding RNAs can regulate function of CSCs. Function of miRNAs in the regulation of CSCs has been mostly assessed in breast cancer and hepatocellular carcinoma. miR-130a-3p, miR-600, miR-590-5p, miR-142-3p, miR-221, miR-222, miR-638, miR-375, miR-31, and miR-210 are among those regulating this feature in breast cancer. Moreover, miR-206, miR-192-5p, miR-500a-3p, miR-125, miR-125b, miR-613, miR-217, miR-194, and miR-494 regulate function of CSCs in hepatocellular carcinoma. DILC, lncTCF7, MUF, HAND2-AS1, MALAT1, DLX6-AS1, HOTAIR, and XIST are among lncRNAs that regulate function of CSCs. In the present paper, we explain the effects of these two classes of non-coding RNAs in the regulation of activity of CSCs.

H19 is an oncofetal transcript with crucial roles in the development and progression of several neoplastic cells. With anti-apoptotic, pro-proliferative, and pro-migratory functions, H19 affects the carcinogenic process from different functional points. In addition, H19 has central roles in the induction of chemoresistance in breast cancer, lung cancer, glioma, liver cancer, and other types of cancers. Induction of EMT, activation of oncogenic signaling pathways, and changes in the tumor microenvironment are among mechanisms of participation of H19 in chemoresistance. Paclitaxel, doxorubicin, tamoxifen, erlotinib, gefitinib, temozolomide, and methotrexate are among therapeutic agents whose efficacy is influenced by the expression of H19. In the present paper, we discuss the impact of H19 in conferring resistance to chemotherapeutic agents in different cancers.

Jun N-terminal Kinase (JNK) signaling pathway is a conserved cascade among species with particular roles in diverse processes during embryogenesis and normal life. These kinases regulate functions of neurons and the immune system by affecting the expression of genes, modulating the arrangement of cytoskeletal proteins, and regulating apoptosis/survival pathways. They are also involved in carcinogenesis. Several miRNAs and lncRNAs have a functional relationship with JNKs. This interaction contributes to the pathogenesis of traumatic brain injury, ulcerative colitis, hepatic ischemia/ reperfusion injury, acute myocardial infarction, and a number of other disorders. Lung cancer, hepatocellular carcinoma, gall bladder cancer, melanoma, and colon cancer are among malignant conditions in which JNK-related miRNAs/ lncRNAs contribute. The current review aims at depicting the functional interaction between JNKs and lncRNAs/ miRNAs and describing the role of these regulatory transcripts in the pathobiology of human disorders.

Nuclear factor-κB (NF-κB) represents a group of inducible transcription factors (TFs) regulating the expression of a great variety of genes implicated in diverse processes, particularly modulation of immune system responses. This TF has functional interactions with non-coding RNAs, constructing a complicated network through which NF-κB, miRNAs, and lncRNAs coordinately regulate gene expression at different facets. This type of interaction is involved in the pathophysiology of several human disorders including both neoplastic disorders and non-neoplastic conditions. MALAT1 and NKILA are among lncRNAs whose interactions with NF-κB have been vastly assessed in different conditions including cancer and inflammatory conditions. In addition, miR-146a/b has functional interactions with this TF in different contexts. Although miRNAs have mutual interactions with NF-κB, the regulatory role of miRNAs on this TF has been more clarified. The aim of the current review is to explore the function of NF-κB-related miRNAs and lncRNAs in these two types of human disorders.

Quercetin is a flavonoid agent detected in fruits and vegetables with anti-inflammatory, antioxidant, and anticancer effects. This flavonoid can suppress cell cycle transition and induce apoptosis in neoplastic cells. Therapeutic effects of quercetin have been assessed in diverse cancers including prostate cancer through the establishment of in vitro and in vivo experiments. Moreover, this agent might prevent the initiation of this type of cancer as it indirectly blocks the activity of promoters of two important genes in the pathogenesis of prostate cancer i.e. androgen receptor (AR) and prostate specific antigen (PSA). Several in vitro investigations have identified the differential influence of quercetin on normal prostate cells versus neoplastic cells, emphasizing its specific cytotoxic effects on cancerous cells. The most appreciated route of quercetin effect on prostate cancer cells is the detachment of Bax from Bcl-xL and the stimulation of caspase families. Besides, quercetin might enhance the effects of other therapeutic options against prostate cancer. For instance, a combination of TNF-related apoptosis-inducing ligand (TRAIL) and quercetin has been recommended as a novel modality for the treatment of prostate cancer. These kinds of strategies might overcome resistance to apoptosis in cancer cells. In the current paper, we summarize the recent data about the preventive and therapeutic influences of quercetin in prostate cancer.

Tumors of the nervous system can be originated from several locations. They mostly have high mortality and morbidity rate. The emergence of resistance to chemotherapeutic agents is a hurdle in the treatment of patients. Long non-coding RNAs (lncRNAs) have been shown to influence the response of glioblastoma/glioma and neuroblastoma to chemotherapeutic agents. MALAT1, NEAT1, and H19 are among lncRNAs that affect the response of glioma/glioblastoma to chemotherapy. As well as that, NORAD, SNHG7, and SNHG16 have been shown to be involved in conferring this phenotype in neuroblastoma. Prior identification of expression amounts of certain lncRNAs would help in the better design of therapeutic regimens. In the current manuscript, we summarize the impact of lncRNAs on chemoresistance in glioma/glioblastoma and neuroblastoma.

The PI3K/AKT pathway is an intracellular signaling pathway with an indispensable impact on cell cycle control. This pathway is functionally related with cell proliferation, cell survival, metabolism, and quiescence. The crucial role of this pathway in the development of cancer has offered this pathway as a target of novel anti-cancer treatments. Recent researches have demonstrated the role of microRNAs (miRNAs) and long noncoding RNAs (lncRNAs) in controlling the PI3K/AKT pathway. Some miRNAs such as miR-155-5p, miR-328-3p, miR-125b-5p, miR-126, miR-331-3p and miR-16 inactivate this pathway, while miR-182, miR-106a, miR-193, miR-214, miR-106b, miR-93, miR-21 and miR-103/107 enhance activity of this pathway. Expression levels of PI3K/AKT-associated miRNAs could be used to envisage the survival of cancer patients. Numerous lncRNAs such as GAS5, FER1L4, LINC00628, PICART1, LOC101928316, ADAMTS9-AS2, SLC25A5-AS1, MEG3, AB073614 and SNHG6 interplay with this pathway. Identification of the impact of miRNAs and lncRNAs in the control of the activity of PI3K/AKT pathway would enhance the efficacy of targeted therapies against this pathway. Moreover, each of the mentioned miRNAs and lncRNAs could be used as a putative therapeutic candidate for the interfering with the carcinogenesis. In the current study, we review the role of miRNAs and lncRNAs in controlling the PI3K/AKT pathway and their contribution to carcinogenesis.

Radiologists frequently diagnose two ureteral duplications including complete and incomplete types. Incomplete ureter duplication, which is also called bifid ureter, refers to a situation in which the ureteric bud bifurcates before meeting the metanephric blastema. On the other hand, complete ureter duplication, which is also named double ureter, defines another situation in which two separate ureteric buds, on either side of the embryonic body, are formed from the mesonephric duct (Wolffian duct) and then arrive in the metanephric blastema. Therefore, two separate ureters, renal pelvis, as well as a duplex kidney (upper and lower poles) are formed in a common renal capsula. Embryologically, in complete ureter duplication, the ureteric buds rotate 108 degrees when incorporating into the urogenital sinus, which is known as Weigert-Meyer rule. In this posture, the upper and lower poles of the kidney are drained by the laterocranial and mediocaudal orifice, respectively. Complete duplication is more common in women than men and is often associated with vesicoureteral reflux, ectopic ureterocele, and/or ectopic ureteral insertion. In the present case report, a 40-year-old woman, mainly complaining of abdominal and lower back pain, was discovered to have bilateral complete ureteral duplication on computed tomography (CT) scan, as well as kidney, ureter, and bladder x-ray radiography. Moreover, the embryological causes were discussed in forming the duplicated ureter and duplex collecting system.

Objectives: Dietary n-3 polyunsaturated fatty acids have positive effects on the heart. The present study investigated the effects of pretreatment with fish oil (FO) and flaxseed oil (FLO) on the heart of the rat, which is associated with the isoprenaline (ISO)-induced myocardial injury. Materials and Methods: The study was conducted on 40 male Wistar rats which were included in control, ISO, FO + ISO, and FLO + ISO groups (each containing 10 rats). In ISO rats, acute myocardial ischemia was induced by ISO while in FO + ISO group, the rats were pretreated with FO orally for 4 weeks. Finally, rats in the FLO + ISO group received pretreatment with FO and flaxseed oil orally for 4 weeks. Eventually, the histopathological examinations of the cardiac tissues and serum activity of creatine kinase-MB (CK-MB) were assessed. Moreover, mitochondria were isolated to examine the mitochondrial swelling. Results: Based on the results, ISO administration significantly increased the serum CK-MB activity compared to the control group. In addition, severe muscular damage to the heart was observed in more than 70% of the rats in ISO group. However, a remarkable decrease in the intensity of heart tissue destruction, as well as the serum levels of CKMB was found in the FO + ISO group compared to the ISO group. Conversely, there was no significant decrease in the serum level of CKMB in FLO + ISO group compared to the ISO group. Conclusions: In general, pretreatment with FLO significantly suppressed the intensity of heart tissue destruction compared to the myocardial ischemic group. FO and FLO led to a decrease in CaCl2-induced swelling in the mitochondria. Therefore, FO and FLO result in protecting against ischemia/reperfusion injury through inhibiting the 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine.

Background: Diabetes is one of the most chronic and widespread diseases causing the damages to the male reproductive system. Nowadays, several studies have been performed to show the role of phenolic compounds in reducing the complications of diabetes. Carvacrol is a phenolic monoterpene which has been shown to have much therapeutic efficacy in various diseases. Methods: Thirty-two adult male Wistar rats (n = 8 in each group) were used in this experimental study. The induction of diabetes was performed using a single intraperitoneal (IP) injection of STZ (50 mg/kg). Rats were assigned into the following groups: control group, diabetic group, diabetic group daily fed with carvacrol at a dose of 75 mg/kg for 8 weeks, and the control group daily fed with carvacrol at a dose of 75 mg/kg for 8 weeks. Results: Treatment with carvacrol significantly improved the histological morphology of the testis, reduced the tissue activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx) enzymes, and diminished the elevated levels of tissue malondialdehyde (MDA) (p < 0.05). Moreover, our results showed that carvacrol significantly decreased Bax and increased Bcl-2 at the levels of gene and protein expression. It also significantly (p

Objective Panax ginseng is a popular traditional herb that has been used in complementary and alternative medicine in eastern Asia, and it possesses pharmacologically active compounds like ginsenosides (GSs). This study aimed to investigate the impact of Panax ginseng extract (PGE) at different concentrations on in vitro follicular function and development in a three-dimensional (3D) culture system fabricated using sodium alginate after 12 days of culture. Materials And Methods In this experimental study, preantral follicles (n=661) were mechanically isolated from the ovaries of 14-day-old female NMRI mice using 29-gauge insulin syringes. Follicles were individually capsulated within sodium alginate, and divided into four groups including control and experimental groups 1, 2, and 3. Then, they were cultured for 12 days in the medium supplemented with different concentrations of PGE (0, 50, 100, and 500 µg/ mL, for control groups and groups 1, 2 and 3, respectively). At the end of the culture period, the mean diameter and maturation of follicles, follicular steroid production, mRNA expression level of proliferating cell nuclear antigen (PCNA) and follicle stimulating hormone receptor (FSH-R), and reactive oxygen species (ROS) levels in collected metaphase-II (MII) oocytes were determined. Results The mean diameter of follicles in group 2 was significantly increased as compared to other groups (P

Objective: To evaluate the impact of Olea (O.) europaea extract on markers of oxidative stress and apoptosis of ovarian tissues in a rat model of torsion/detorsion-induced ovarian damage. Methods: A total of 28 Wistar female rats were randomly assigned into 4 groups, with 7 rats in each group. The sham group received a 2.5 cm longitudinal incision in the midline part of the abdomen which was then sutured with 5-0 nylon thread; the torsion/detorsion group underwent torsion induction for 3 h followed by reperfusion for 10 days; the torsion/detorsion+O. europaea group received 300 mg/kg hydro-alcoholic extract of O. europaea 30 min before detorsion, followed by reperfusion for 10 days; and the O. europaea group only received 300 mg/kg hydro-alcoholic extract of O. europaea for 10 days. After the treatment period, blood samples were taken; the levels of estrogen, glutathione peroxidase, superoxide dismutase, and malondialdehyde were assayed. The histological changes, as well as the rate of apoptosis in ovarian tissues, were also carried out by histomorphometric analysis at day 10 post-procedure. Results: Histological comparisons demonstrated a significant detrimental change in the torsion/ detorsion group as compared with other groups. The number of pre-antral and antral follicles and corpus luteum was significantly decreased in the torsion/detorsion group compared with the sham group, while treatment with O. europaea could enhance their numbers (P

5-fluorouracil (5-FU) is among the mostly administrated chemotherapeutic agents for a wide variety of neoplasms. Non-coding RNAs have a central impact on the determination of the response of patients to 5-FU. These transcripts via modulation of cancer-related pathways, cell apoptosis, autophagy, epithelial–mesenchymal transition, and other aspects of cell behavior can affect cell response to 5-FU. Modulation of expression levels of microRNAs or long non-coding RNAs may be a suitable approach to sensitize tumor cells to 5-FU treatment via modulating multiple biological signaling pathways such as Hippo/YAP, Wnt/β-catenin, Hedgehog, NF-kB, and Notch cascades. Moreover, there is an increasing interest in targeting these transcripts in various kinds of cancers that are treated by 5-FU. In the present article, we provide a review of the function of non-coding transcripts in the modulation of response of neoplastic cells to 5-FU.

The extracellular matrix (ECM) creates a multifaceted system for the interaction of diverse structural proteins, matricellular molecules, proteoglycans, hyaluronan, and various glycoproteins that collaborate and bind with each other to produce a bioactive polymer. Alterations in the composition and configuration of ECM elements influence the cellular phenotype, thus participating in the pathogenesis of several human disorders. Recent studies indicate the crucial roles of non-coding RNAs in the modulation of ECM. Several miRNAs such as miR-21, miR-26, miR-19, miR-140, miR-29, miR-30, miR-133 have been dysregulated in disorders that are associated with disruption or breakdown of the ECM. Moreover, expression of MALAT1, PVT1, SRA1, n379519, RMRP, PFL, TUG1, TM1P3, FAS-AS1, PART1, XIST, and expression of other lncRNAs is altered in disorders associated with the modification of ECM components. In the current review, we discuss the role of lncRNAs and miRNAs in the modification of ECM and their relevance with the pathophysiology of human disorders such as cardiac/ lung fibrosis, cardiomyopathy, heart failure, asthma, osteoarthritis, and cancers.

The insulin-like growth factors (IGFs) are polypeptides with similar sequences with insulin. These factors regulate cell growth, development, maturation, and aging via different processes including the interplay with MAPK, Akt, and PI3K. IGF signaling participates in the pathogenesis of neoplasia, insulin resistance, diabetes mellitus, polycystic ovarian syndrome, cerebral ischemic injury, fatty liver disease, and several other conditions. Recent investigations have demonstrated the interplay between non-coding RNAs and IGF signaling. This interplay has fundamental roles in the development of the mentioned disorders. We designed the current study to search the available data about the role of IGF-associated non-coding RNAs in the evolution of neoplasia and other conditions. As novel therapeutic strategies have been designed for modification of IGF signaling, identification of the impact of non-coding RNAs in this pathway is necessary for the prediction of response to these modalities.

Epithelial to mesenchymal transition (EMT) is a course of action that enables a polarized epithelial cell to undertake numerous biochemical alterations that allow it to adopt features of mesenchymal cells such as high migratory ability, invasive properties, resistance to apoptosis, and importantly higher-order formation of extracellular matrix elements. EMT has important roles in implantation and gastrulation of the embryo, inflammatory reactions and fibrosis, and transformation of cancer cells, their invasiveness and metastatic ability. Regarding the importance of EMT in the invasive progression of cancer, this process has been well studies in in this context. Non-coding RNAs (ncRNAs) have been shown to exert critical function in the regulation of cellular processes that are involved in the EMT. These processes include regulation of some transcription factors namely SNAI1 and SNAI2, ZEB1 and ZEB2, Twist, and E12/E47, modulation of chromatin configuration, alternative splicing, and protein stability and subcellular location of proteins. In the present paper, we describe the influence of ncRNAs including microRNAs and long non-coding RNAs in the EMT process and their application as biomarkers for this process and cancer progression and their potential as therapeutic targets.

MicroRNA-124 (miR-124) is a copious miRNA in the brain, but it is expressed in a wide range of human/animal tissues participating in the pathogenesis of several disorders. Based on its important function in the development of the nervous system, abnormal expression of miR-124 has been detected in nervous system diseases including Alzheimer's disease, Parkinson's disease, Hypoxic-Ischemic Encephalopathy, Huntington's disease, and ischemic stroke. In addition to these conditions, miR-124 contributes to the pathogenesis of cardiovascular disorders, hypertension, and atherosclerosis. Besides, it has been shown to be down-regulated in a wide range of human cancers such as colorectal cancer, breast cancer, gastric cancer, glioma, pancreatic cancer, and other types of cancer. Yet, few studies have reported upregulation of miR-124 in some cancer types. In the current study, we describe the role of miR-124 in these malignant and non-malignant conditions.

Twist-related protein 1 (Twist1) is a basic helix-loop-helix (bHLH) transcription factor (TF) being coded by the TWIST1 gene. This TF has a fundamental effect on the normal development and in the pathogenesis of various diseases especially cancer. Twist1 has interactions with some long non-coding RNAs and miRNAs. The interactions between this TF and various miRNAs such as miR-16, miR-26b-5p, miR-1271, miR-539, miR-214, miR-200b/c, miR-335, miR-10b, and miR-381 are implicated in the carcinogenic processes. TP73-AS1, LINC01638, ATB, NONHSAT101069, CASC15, H19, PVT1, LINC00339, LINC01385, TANAR, SNHG5, DANCR, CHRF, and TUG1 are among long non-coding RNAs which interact with Twist1 and participate in the carcinogenesis. This review aims at depicting the interaction between these non-coding transcripts and Twist1 and the consequence of these interactions in human neoplasms.

MicroRNA-140 (miR-140) has been shown to be associated with the pathogenesis of a wide range of pathologies including osteoarthritis, osteoporosis, renal fibrosis, ischemic conditions, and most importantly neoplasia. This miRNA has been shown to be down-regulated in a diversity of cancers namely breast cancer, gastrointestinal cancers, lung cancer, and prostate cancer. miR-140 has a lot of immune-related targets. Moreover, several miR-140 targets regulate cell proliferation, cell cycle transition, and apoptosis. This miRNA has been shown to be sponged by a number of lncRNAs and circ-RNAs. miR-140 has essential roles in the determination of the sensitivity of neoplastic cells to chemotherapeutic agents such as temozolomide, doxorubicin, and cisplatin. Besides, expression quantities of miR-140 in cancer tissues can be used for the prediction of clinical outcomes of patients with neoplasia. In the present paper, we describe the impact of miR-140 in neoplastic and non-neoplastic disorders.

Paclitaxel is a chemotherapeutic substance that is administered for treatment of an extensive spectrum of human malignancies. In spite of its potent short-term effects against tumor cells, resistance to paclitaxel occurs in a number of patients precluding its long-term application in these patients. Non-coding RNAs have been shown to influence response of cancer cells to this chemotherapeutic agent via different mechanisms. Mechanistically, these transcripts regulate expression of several genes particularly those being involved in the apoptotic processes. Lots of in vivo and in vitro assays have demonstrated the efficacy of oligonucleotide-mediated microRNAs (miRNA)/ long non-coding RNAs (lncRNA) silencing in enhancement of response of cancer cells to paclitaxel. Therefore, targeted therapies against non-coding RNAs have been suggested as applicable modalities for combatting resistance to this agent. In the present review, we provide a summary of studies which assessed the role of miRNAs and lncRNAs in conferring resistance to paclitaxel.