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Lung cancer is the most common type of cancer in our country and worldwide, and it is a leading cause of cancer-related deaths. According to the latest global cancer statistics, lung cancer was identified as the second most common type of cancer, and the leading cause of cancer-related deaths. Long non-coding RNAs (lncRNAs) are a highly heterogeneous class of RNA molecules sharing many characteristics with mRNAs, except for the protein-coding potential. Accumulating mass of evidence suggest that lncRNAs play key regulatory roles during the multistep formation of human cancers including lung cancer. In previous studies, it has been shown that many lncRNA molecules play significant roles in the formation and progression of lung cancer. However, there are still numerous lncRNA molecules in lung cancer whose roles remain unknown. Accordingly, here we sought to ascertain the diagnostic and prognostic value of lncRNAs by analyzing the expression profiles of THRIL, NEAT1, and LOC105376095 in lung cancer. Remarkably, NEAT1 and LOC105376095 but not THRIL were identified to be differentially expressed in tissues of lung tumors. More importantly, LOC105376095, a yet uncharacterized lncRNA molecule, was significantly associated with the disease severity. Collectively, NEAT1 and LOC105376095 hold promise as potential diagnostic and prognostic biomarkers for lung cancer, presenting opportunities for targeted therapeutic interventions in the future., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Lung cancer, known for its high mortality rates and poor prognosis, remains one of the most prevalent cancer types. Early detection and effective treatment methods are crucial for improving survival rates. Non-small cell lung cancer (NSCLC) accounts for approximately 85 % of all lung cancer cases. Long non-coding RNAs (lncRNAs), which play vital roles in various biological processes, have been implicated in the development of cancer and can impact key therapeutic targets in different cancer types. In NSCLC, the dysregulation of specific lncRNAs, such as MALAT1 and NORAD, has been associated with neoplastic initiation, progression, metastasis, tumor angiogenesis, chemoresistance, and genomic instability. Both MALAT1 and NORAD directly regulate the expression of the transcription factor E2F1, thereby influencing cell cycle progression. Additionally, MALAT1 has been reported to affect the expression of p53 target genes, leading to cell cycle progression through the repression of p53 promoter activity. NORAD, on the other hand, is indirectly regulated by p53. The AT-rich interaction domain (ARID) family of DNA-binding proteins, particularly ARID3A and ARID3B, are involved in various biological processes such as cell proliferation, differentiation, and development. They also play significant roles in E2F-dependent transcription and are transcriptional targets of p53. The intricate balance between promoting cellular proliferation through the pRB-E2F pathway and inducing growth arrest through the p53 pathway underscores the crucial regulatory role of ARID3A, ARID3B, and their interaction with lncRNAs MALAT1 and NORAD. In this study, we aimed to investigate the potential interactive and functional connections among ARID3A, ARID3B, MALAT1, and NORAD in NSCLC, considering their involvement in the pRB-E2F and p53 pathways. Our findings strongly suggest that ARID3A and ARID3B play a regulatory role in controlling MALAT1 and NORAD in NSCLC. Specifically, our study demonstrates that the activities of MALAT1 and NORAD were markedly increased upon the overexpression of ARID3A and ARID3B. Therefore, we can conclude that ARID3A and ARID3B likely contribute significantly to the oncogenic functions of MALAT1 and NORAD in NSCLC. Consequently, targeting ARID3A and ARID3B could hold promise as a therapeutic approach in NSCLC, given their direct control over the expression of MALAT1 and NORAD., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Fibrosis is a pathological wound-healing mechanism that results by the overactivation of fibroblasts. Fibrosis can become obstructive and deleterious during regeneration of various body tissues including cardiac muscle. This ultimately results in the development of cardiac fibrosis, characterized by an excessive buildup of extracellular matrix proteins. Thus, it could lead to arrhythmias and heart failure which creates a leading public health burden worldwide. MiRNAs are small non-coding RNAs with great potential for diagnostic and therapeutic purposes. Mounting evidence indicates that miRNAs are involved in the deregulation of tissue homeostasis during myocardial fibrosis. For instance, miRNAs that are implicated in the regulation of TGF-beta signaling pathway have been reported to be significantly altered in myocardial fibrosis. Accordingly, in this comprehensive review, we discuss and highlight recent available data on the role of miRNAs during myocardial fibrosis, providing valuable insights into the miRNA modulation of cardiac fibrosis and miRNAs targets that can be used in the future therapeutic interventions to cardiac fibrosis., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

In the Mid-19 th century, Rudolf Virchow considered necrosis to be a prominent form of cell death; since then, pathologists have recognized necrosis as both a cause and a consequence of disease. About a century later, the mechanism of apoptosis, another form of cell death, was discovered, and we now know that this process is regulated by several molecular mechanisms that "programme" the cell to die. However, discoveries on cell death mechanisms are not limited to these, and recent studies have allowed the identification of novel cell death pathways that can be molecularly distinguished from necrotic and apoptotic cell death mechanisms. Moreover, the main goal of current cancer therapy is to discover and develop drugs that target apoptosis. However, resistance to chemotherapeutic agents targeting apoptosis is mainly responsible for the failure of clinical therapy and adverse side effects of the chemotherapeutic agents currently in use pose a major threat to the well-being and lives of patients. Therefore, the development of natural-based anticancer drugs with low cellular and organismal side effects is of great interest. In this comprehensive review, we thoroughly examine and discuss natural anticancer compounds that specifically target non-canonical cell death mechanisms., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Radicular cysts are characterized by significant levels of changes in inflammatory biomarkers. Among them, interleukins and growth factors have been reported to be deregulated in radicular cyst tissues. Moreover, long non-coding RNAs are recently discovered non-coding RNA molecules that regulate various intracellular stimuli to keep homeostasis in balance. A growing body of evidence suggests that lncRNAs are significantly involved in the regulation of inflammation by targeting various inflammatory biomarkers. Accordingly, the present study was aimed to investigate the gene expression levels of inflammation-related lncRNAs in radicular cysts and show their possible roles in the development of radicular cysts. For the study, a total of 25 patients with a radiologically and pathologically confirmed radicular cyst were enrolled. For the determination of non-coding RNA expression levels, real-time qPCR was used. As a result of the current study, expression levels of PACER and THRIL were found to be significantly elevated in radicular cyst tissues compared to control tissue samples. However, MALAT1, ANRIL, and NEAT1 expression levels were not significantly altered in radicular cyst tissues compared to control tissue samples. In conclusion, long non-coding RNAs, PACER and THRIL, seem to have significant pathophysiological roles by acquiring molecular changes during inflammation and might be involved in the development and formation of radicular cysts., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Advances in high-throughput genomic technologies have enabled the identification of numerous selective tumor markers. However, adapting these newly identified markers to clinical practice is not always possible because most RNA molecules, including mRNAs of protein-coding genes and long non-coding RNAs, are not stable under laboratory conditions, making their testing a major challenge. In contrast to long RNA molecules, miRNAs offer a great advantage in that they are relatively stable due to their small size. Accordingly, herein we aimed to determine the expression levels of miRNAs that are involved in Wnt/β-catenin signaling pathway in formalin fixed paraffin embedded (FFPE) tissue samples of patients with salivary gland tumors. A total of 42 patients with salivary gland tumors were included in the study. The miRNA expression signatures were evaluated using the RT-qPCR. As a result, β-catenin positivity was observed in all salivary gland tumors without distinguishing between benign and malignant phenotypes. Remarkably, we found that miR-200a and miR-373 were significantly upregulated whereas miR-30c were downregulated in tissues of patients with salivary gland tumors, compared to adjacent healthy tissue samples. In addition, distinct expression signatures of these miRNAs were significantly associated with the clinicopathological findings of patients such as perineural invasion and lymph node metastasis. Additionally, miR-145 and miR-30a were found to be specifically downregulated in a mucoepidermoid carcinoma. Also, miR-26b was selectively increased in pleomorphic adenomas of the salivary gland. Collectively, our findings suggest that these miRNAs may play chief roles in the differential diagnosis of salivary gland tumors., Competing Interests: Declaration of Competing Interest The authors declare that they have no conflict of interest., (Copyright © 2022 Elsevier GmbH. All rights reserved.)

Cancers of the lips and oral cavity are a leading cause of death worldwide. Although they account for only 2% of the global cancer burden, they significantly affect the comfort of patients and eventually lead to a person's death. Also, defects in the cellular stress response and apoptosis mechanisms regulated by p53 activity is an important hallmark of cancer cells. Here, we aimed to decipher miRNAs associated with cellular stress response and apoptosis mechanisms regulated by p53 activity in patient with lower lip cancer and reveal the association of these miRNAs with the clinical course of the disease. The present research included a total of 40 eligible individuals with pathologically confirmed lower lip cancer diagnosis. Formalin-fixed, paraffin-embedded (FFPE) tissue samples of patients were obtained, and miRNAs expressions were analyzed by qPCR. Immunohistochemistry was used to determine p53 and Ki67 expression status. While three of these miRNAs (miR-130a, -375, and -128a) were found to be elevated in tumor cells compared to normal tissues of lower lip cancer patients, five were downregulated (let-7a, -7b, -7c, and miR-138, -23a), but only three were significantly altered. Particularly, we identified three miRNA signatures in which miR-128a was significantly upregulated and miR-23a and let-7c were significantly downregulated in patients with lower lip cancer. Remarkably, let-7c identified to be a promising prognostic factor for lip cancer. Our findings demonstrate that these miRNAs play important regulatory roles in lower lip cancer pathobiology, highlighting their potential relevance in diagnosis and prognosis of these patients. Moreover, these miRNAs can be targeted in future therapeutic interventions against lower lip cancer., (Copyright © 2022 Elsevier GmbH. All rights reserved.)