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For a graph G=(V,E), a triple Roman dominating function (3RD-function) is a function f:V→{0,1,2,3,4} having the property that (i) if f(v)=0 then v must have either one neighbor u with f(u)=4, or two neighbors u,w with f(u)+f(w)≥5 or three neighbors u,w,z with f(u)=f(w)=f(z)=2, (ii) if f(v)=1 then v must have one neighbor u with f(u)≥3 or two neighbors u,w with f(u)=f(w)=2, and (iii) if f(v)=2 then v must have one neighbor u with f(u)≥2. The weight of a 3RDF f is the sum f(V)=∑v∈Vf(v), and the minimum weight of a 3RD-function on G is the triple Roman domination number of G, denoted by γ[3R](G). In this paper, we prove that for any connected graph G of order n with minimum degree at least two, γ[3R](G)≤3n2. [ABSTRACT FROM AUTHOR]

BACKGROUND: Colorectal cancer (CRC), is the third most common cancer type. MicroRNAs and their roles in cancer progression have gained considerable attention in the scientific community. miR-485-3p has been identified to be abnormally expressed in different types of cancer, but its expression level, biological function, and underlying pathways are still unclear in CRC. Targeting Protein for Xenopus kinesin-like protein 2 (TPX2) is a nuclear protein which plays vital roles in cancer progression and mitotic spindle assembly. TPX2 is overexpressed in various malignancies and has been predicted as an indirect target of miR-485-3p. This study aims to investigate the miR-485-3p and TPX2 expression level, their potential correlation, and underlying molecules like P53 and P21 in forty-one pairs of colorectal cancer tissues compared to matched non-cancerous ones. MATERIALS AND METHODS: We used forty-one pairs of CRC fresh tissue samples and their adjacent normal ones for RNA extraction. After cDNA synthesis, the expression level of miR-485-3p, TPX2, P53 and P21 were determined by Real-time PCR. RESULTS AND CONCLUSIONS: The results revealed that miR-485-3p was significantly downregulated and TPX2 was highly upregulated in CRC tissues. Moreover, miR-485-3p was negatively correlated with TPX2 expression and positively correlated with P21 expression. We present miR-485-3p as a suppressor for colorectal cancer (Tab. 2, Fig. 8, Ref. 44). Text in PDF www.elis.sk. [ABSTRACT FROM AUTHOR]

The World Health Organization has considered the infertility as an international public health problem. Infertility affect nearly 1 in 7 couples and male component contributes to 50% of infertility cases. There is a clear link between male infertility and some cancers such as testicular germ cell, prostate and colon cancers. Two possibilities support this finding: 1) Cancer treatments can affect the fertility factors 2) Genetic profile of infertility genes have been altered in cancer patients. Although the previously published researches have mostly focused on the first factor, no article has yet confirmed the role of genetic factors. In this in silico study, we collected the large number of genes ( n  = 17703) involved in infertility. These genes were collected from NGS panel tests of male infertility and comprehensive literature review or online data base. The Prostate Adenocarcinoma genomic and transcriptomics raw data were downloaded from the cBioPortal Cancer dataset. This included with 494 patients of Prostate Cancer with 494 mutation data, 489 with CNA and 493 with RNA seqV2 data. TCGA RNA-Seq raw data was extracted in R using the cgdsr extension package with a threshold of ±2 relative to normal samples. The observed data showed that male infertility genes have been distributed through the human genome. Among the 17703 analyzed genes of this study, the genomic profile of three genes including OR9Q1, H4C6 and PSG7 were changed approximately in 100% of ( n  = 493) patients. In most of patients (>98%), genetic alteration was related to change in gene expression. In conclusion, this study showed that the genomic and transcriptomics patterns of some male-infertility genes are notably altered in patients of prostate cancer and suggested a possible role of genetic factors in occurrence of infertility in cancer patients. Our information can be used as a source for the design of genetic database of male-infertility.

Background: Mesenchymal stem cells (MSC) are a type of multipotent stem cell whose differentiation into cartilage cells has been considered in recent years. Platelet-rich plasma (PRP) may impair cartilage differentiation due to its richness in growth factors and hyperosmolarity due to its proximity to the required cartilage environment., Objectives: The main purpose of this study was to treat human adipose tissue-derived MSCs concurrently with PRP and hyperosmolarity to investigate the expression profile of micro-RNA (miRNA) involved in the cartilage process differentiation. We examined the effect of PRP and the increase in osmolarity on the expression of miR-27, miR-101, miR-140, miR-145, miR-146, and miR-199., Methods: Mesenchymal stem cells were extracted from human adipose tissue and differentiated into chondrocytes and the effect of baseline cultures (diff), PRP (prp), hyperosmolarity (os), base plus hyperosmolarity (diff + os), PRP plus hyperosmolarity (prp + os) next to the control group were studied in cartilage differentiation using specific stains such as Alcian blue, hematoxylin and eosin, and collagen type 2 and 10 immunohistochemistry. In addition, the expression of miR-27, miR-140, miR-199, miR-146, miR-101, and miR-145 was evaluated using real-time PCR., Conclusion: Human adipose tissue-derived MSCs with the ability to differentiate into adipocytes and osteocytes showed the properties of chondrocytes in all differentiation groups. Alkaline phosphatase (ALP) enzyme activity and calcium deposition were lower in the diff + os group than in other groups. Therefore, the diff + os group may be a more suitable environment for cartilage differentiation. Furthermore, 5% PRP concentration and hyperosmolarity showed a positive effect on miR-140, miR-199, miR-27, and, miR-146 and a negative effect on miR-101 and miR-145 on cartilage differentiation., 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. Published by Elsevier B.V.)

Background: Gastric cancer (GC) is the fourth most common human malignancy and the second reason for cancer morbidity worldwide. Long noncoding RNA (LncRNA) HOX transcript antisense RNA (HOTAIR) has recently emerged as a promoter of metastasis in various cancer types, including GC, through the epithelial‑mesenchymal transition (EMT) process. However, the exact mechanism of HOTAIR in promoting EMT is unknown. Aberrant expression of the miR-200 family has been linked to the occurrence and development of various types of malignant tumors. This study investigates the correlation between the HOTAIR and miR-200 family gene expression patterns in GC cell lines. We investigated the miR-200 and HOTAIR due to their common molecular features in the EMT process., Methods: AGS and MKN45 cell lines were transfected with si-HOTAIR, along with a negative control. The effect of HOTAIR knockdown was also analyzed on cell viability and also on the expression of miR-200 family members, including miR-200a, -200b, and -200c, in cell lines using qRT-PCR. Statistical analysis was performed to find the potential correlation between the expression level of HOTAIR and miRs., Results: Our results showed significant increased miR-200 family expression level in transfected AGS and MKN45 GC cells (fold changes > 2; p < 0.001). Moreover, a negative correlation was observed between HOTAIR and miR-200 expression levels in GC cell lines (p < 0.05)., Conclusion: Our findings showed a significant association between miR-200 family and HOTAIR expression levels in GC cell lines. Taken together, the HOTAIR-miR-200 axis seems to play a vital role in human GC, suggesting a potential therapeutic target in future GC treatment.

Background: The global incidence of colorectal cancer (CRC) is expected to be increased by 60% until a few years. Despite the advances in surgical and chemotherapy techniques, a significant proportion of patients with CRC have poor responses to treatments. These are the reasons that prove the importance of identifying molecular bio-markers as potential therapeutic targets. Long non-coding RNAs (lnc RNAs) participate in the initiation, development, progression, and metastasis of cancers such as CRC. Hence, this class of noncoding RNAs is known as bio-marker for cancer dia-gnosis and prognosis., Materials and Methods: In this experimental study, the extraction of total RNA from tissues, synthesis of complementary DNA as well as quantitative real-time polymerase chain reaction (qRT- PCR) were performed. Comparative cycle threshold method was applied to quantify the expression level of lncRNA-SNHG7 and FAIM2. The relative amount of lncRNA-SNHG7 and FAIM2 was calculated using the equation 2 -DDCT., Results: In this study, by qRT PCR, we concluded that the expression level of SNHG7, as a recently identified lncRNA and FAIM2 were increased in colorectal cancer tissues compared with normal adjacent tissues., Conclusion: Our study indicates the potential importance of SNHG7 and FAIM2 expression for more studies in future.

Intellectual disability (ID) is characterized by significant deficits in adaptive behaviors and cognitive functioning. The involvement of both genetic and environmental factors in pathogenesis of the ID, makes the diagnosis of the disease more complicated. Nowadays, the entrance of next generation sequencing (NGS) approaches has facilitated the discovery of causative genes in this genetically heterogeneous disease. Here, we report a novel nonsense mutation (c.115 C > T, p.Gln39X) of INPP4A gene in a family with inherited ID using whole exome sequencing (WES). The mutation was completely co-segregated with disease phenotype in all affected members, and unaffected members of family were either homozygous or heterozygous. In silico analysis predicted the c.115 C > T; p.Gln39X as probably pathogenic variant. It seems that mutated transcript would degrade through nonsense-mediated decay (NMD) or potentially form strongly truncated protein lacking functionally important domain like C2A&#95;copine. The INPP4A is an important neuroprotective protein which is preferentially detected in brain. The variant c.115C > T; p.Gln39X is the third reported mutation of INPP4A gene in neurological diseases. Such variants further expand the mutation spectrum in INPP4A and substantiate its role in the pathogenesis of ID. However, more experimental data are needed for considering these mutations in genetic counseling., Competing Interests: Declaration of competing interest The authors declare no conflict of interest., (Copyright © 2020 Elsevier Masson SAS. All rights reserved.)

Colorectal cancer (CRC) is one of the most common types of cancer worldwide. However, the molecular mechanisms involved in CRC initiation and progression is remained to be unknown. It seems that lncRNAs, as the main and lengthy functional transcripts of the genome, have important roles in different cancers such as CRC. CRC-related lncRNAs are reported to be involved in diverse molecular processes such as metastasis, invasion, cell proliferation, and apoptosis. This study was aimed to analyse the expression level of lncRNA SNHG1 in colorectal adenocarcinoma and normal tissues. We performed an in silico analysis on a large cohort and confirmed the results by experimental analysis of clinical samples through real-time PCR. Our findings demonstrated that that SNHG1 is potentially overexpressed in tumor tissues compared with adjacent normal tissues. The expression level of SNHG1 was shown to be potentially associated with clinicopathological features of tumors. The current study suggests the potential role of SNHG1 in colon cancer progression.

Long noncoding RNAs (lncRNAs) are lengthy noncoding transcripts which are involved in critical signaling pathways including cell cycle and apoptosis so it is not surprising to see their altered expression in human tumors. Colorectal adenocarcinoma is one the most frequent malignancies worldwide. The role of lncRNAs in colorectal adenocarcinoma is not well understood. To study the significance of lncRNAs in colorectal adenocarcinoma, we retrieved 189 approved lncRNAs from HGNC. The genes were imported into the cBioPortal database for transcriptomic analyses. We queried all the samples from TCGA provisional colorectal adenocarcinoma with RNA-seq v2 data in our study and considered RNA dysregulation with Z-score: ±2. The lncRNA which was altered in most of the patients were considered as "significant lncRNA" for further analyses. We considered the association of candidate lncRNAs with clinicopathologic parameters of samples including tumor disease anatomic site, neoplasm histologic types, tumor stage and survival. We also compute the specificity of the significant lncRNAs expression in colorectal adenocarcinoma comparing with other human cancers in cancer portal. Our analysis showed that lncRNAs SNHG6, PVT1 and ZFAS1 allocated the maximum alteration among the colorectal cases. The expression of SNHG6 and ZFAS1 was more in rectal adenocarcinoma than the colon carcinoma while the PVT1 showed the same expression levels in both tissues. However, we found that upregulation of PVT1 has been reduced the overall survival in patients. Altogether these data showed SNHG6, PVT1 and ZFAS1, are promising candidates for experimental research on colorectal adenocarcinoma to discover novel biomarker for this prevalent cancer.

Autosomal recessive cerebellar ataxia is heterogeneous inherited neurodegenerative disorders with more than 70 involved genes. The development of next generation sequencing opens a new window in rapid diagnosis of such heterogeneous condition in medical genetics laboratories. Here, we present ADCK3; del.CD (229-230) mutation in an Iranian consanguineous family with three cerebellar ataxic boys using whole exome sequencing. The mutation was predicted pathogenic and all the affected individuals were homozygous for the variant. Although, the ADCK3 was previously reported as one of the master genes of ARSC, our mutation was novel as has been not previously reported in dbSNP or literature., (Copyright © 2019. Published by Elsevier B.V.)

Background: Short-stature (SS) is multifactorial pathologic condition that originates from either genetic or environmental factors. The diagnosis is based on family history, clinical findings, radiological examination and genetic analysis. A variety of genes have been reported for SS, among which FGFR-3 was the main gene in achondroplasia and hypochondroplasia. In other forms of SS, the gene involved varies from one patient to another. Whole exome sequencing (WES) and comparative genomic hybridization (CGH) have recently introduced a growing body of genes annually. The present study performed a WES analysis on an Iranian family suffering from an inherited form of SS aiming to diagnose the causative gene. The father and all of his four sons were diagnosed as SS., Methods: The blood samples were collected from the proband and his available family members. Genomic DNA was extracted using salting-out method. The DNA of the proband was analyzed using WES and confirmed through polymerase chain reaction (PCR)-sequencing. The WES-extracted variant was evaluated in silico using software aiming to determine whether this nucleotide change is pathogenic. The presence of the variant was traced in other affected family members using PCR-sequencing., Results: Following segregation analysis, variant c.896 G>A of the COMP gene was found in all of the affected individuals in a heterozygous form. This variant resulted in substitution of glycine 299 with arginine and was previously predicted as pathogenic in the Human Gene Mutation Database dataset, although it represents the first report in Iran., Conclusions: The findings of the present study suggest consideration of the c.896 G>A variant of the COMP gene with respect to the genetic counseling of inherited skeletal dysplasia in Iran., (© 2019 John Wiley & Sons, Ltd.)

Objective and Background: Histological and molecular information and biopsy help in the diagnosis of the type and grade of tumors and increase the value of estimation of the biological behavior of tumors. In this study, we focused on a consanguineous Iranian Family with high prevalence of brain tumors in their pedigree and reviewed the literature on MSH6 mutations in brain tumors and the treatment responses focused on Gliomas., Method: We chose a family with a high prevalence of brain tumor in their pedigree. We studied the proband's neuroimaging and brain proton magnetic resonance spectroscopy (MRS), magnetic resonance imaging (MRI), biopsy result, and whole-genome sequencing., Result: The neuroimaging and brain proton MRS reported a lesion in the right frontoparietal. The MRI revealed a large enhancible heterogenous mass in the right temporo-fronto-parieto-occipital lobes with involvement of corpus callosum which was suggestive of glioma. The patient revealed a homozygous pattern for a novel 9 base-pare deletion at the 912-914 codon on exon 4 of the MSH6 gene., Discussion: We discuss several studies on MSH6 mutations in brain tumors and we discuss treatment responses in MSH6 mutations and the studies conducted to sensitize chemotherapy and radiotherapy resistance brain tumors to face this subject efficiently., Conclusion: Patients should be evaluated for MMR mutation before chemo and radiotherapy, and it is valuable to follow-up these mutations during the treatment too. In temozolomide (TMZ)-resitance cases, it is suggested to use complementary strategies such as using HDACis and a combination of a STAT3 Inhibitor and an mTOR inhibitor, BER inhibition mechanism, and PARP-1 inhibitor., (© 2018 Wiley Periodicals, Inc.)

Objectives: Charcot-Marie Tooth disease (CMT) is one of the main inherited causes of motor and sensory neuropathies with variable expressivity and age-of onset. Although more than 70 genes have been identified for CMT, more studies are needed to discover other genes involved in CMT. Introduction of whole exome sequencing (WES) to capture all the exons may help to find these genes., Materials and Methods: Here, we tried to find the genetic cause of the neuropathy in two Iranian brothers using WES. Blood sample was collected from probands and their family members to extract the genomic DNA. The extracted DNA from one of the affected case was subjected for WES. The variant calls were filtered to reveal the pathogenic variant. Presence of the candidate mutation was confirmed using Sanger sequencing. The pathogenic potential of the variant was examined using in silico software. Using ClustalW multiple alignment, the presence of variant in conserved domain of protein was investigated. The parent and another affected boy were also checked for presence of the variant using PCR-sequencing., Results: The obtained data presented a novel TTC del mutation in CDS 738 of dystrophin related protein 2 ( DRP2 ) gene, which was validated by sequencing. The variant was located in a conserved domain of DRP2 protein and predicted as pathogenic. Two affected boys were hemizygous for the mutation and received the mutation from mother., Conclusion: Here, we provided the evidence for the contribution of DRP2 in CMT. Also, the symptoms shed light on molecular aspect of this genetically heterogeneous disease.

Objectives: The non-coding RNA rprA can increase the resistance to ampicillin in Escherichia coli., Methods: Bacterial DNA was extracted by boiling method and then amplified using polymerase chain reaction (PCR) with two different primer sets. Recombinant pET28a/rprA-sense and -antisense plasmids were separately transferred into the competent E. coli BL21 (DE3) by chemical methods using heat shock. The expression was analyzed at the RNA level using Semi quantitative RT PCR. The turbidity difference between the bacteria was checked by Broth Dilution method., Results: The statistical analysis showed that the turbidity difference between the up regulated and control bacteria is significant (p value < 0.0001). The ANOVA test also showed the significant difference between the down regulated and control bacteria (p value < 0.0001)., Conclusion: Considering this mechanism, there are some reports indicating the role of rprA in antibiotic resistance. However, the role of rprA in ampicillin resistance is remained to be unknown. The aim of this study was to analyze the up regulation and down regulation of rprA and check their effects on ampicillin resistance in Escherichia coli. It was found that the up regulation and down regulation of rprA can lead into more antibiotics resistance and susceptibility, respectively. Our results showed the potential role of rprA expression in the response to ampicillin stress in E. coli., (Copyright © 2019. Published by Elsevier Ltd.)

Coronary artery disease (CAD) is one of the leading causes of death and disability all around the world. Recent studies have revealed that aberrantly regulated long non-coding RNA (lncRNA) as one of the main classes of cellular transcript play a key regulatory role in transcriptional and epigenetic pathways. Recent reports have demonstrated circulating long noncoding RNAs in blood can be potential biomarkers for CAD. HOTAIR is one of the most cited lncRNAs with a critical role in initiation and progression of the gene expression regulation. Recent research on the role of the HOTAIR in cardiovascular disease lays the basis for the development of new studies considering this lncRNA as a potential biomarker and therapeutic target in CAD. In this study, we aimed to compare the expression of HOTAIR lncRNA in the blood samples of patients with CAD and control samples. The expression level was examined by semi-quantitative reverse transcriptase polymerase chain reaction technique. Our data show that expression of HOTAIR is up-regulated in blood samples of patients with CAD.

Long non-coding RNAs (lncRNAs), are lengthy noncoding transcripts with pivotal roles in biological pathways including cell cycle, apoptosis and chromatin remodeling. Aberrant expression of lncRNAs has been strongly connected with tumor progression and metastasis. However, the prognostic significance of lncRNAs in diffuse large-B-cell lymphoma (DLBCL) remains unclear. In this study, the expression levels of 189 approved lncRNAs were considered in DLBCL patients using several different genomic and transcriptome datasets. The analyses showed that the lncRNA GAS5 allocated the maximum score of RNA dysregulation and can be considered as good choice in DLBCLs' researches., (Copyright © 2018 Elsevier GmbH. All rights reserved.)

Doxorubicin (Dox) is a widely used powerful chemotherapeutic component for cancer treatment. However, its clinical application has been hampered due to doxorubicin-induced cardiomyopathy upon the cessation of chemotherapy. Previous studies revealed that PPARγ plays a crucial protective role in cardiomyocytes. Modulation of miRNA expression is an applicable approach for prohibition of toxicity induction. Therefore, the aim of present study is uprising of PPARγ transcript levels via manipulation of miRNAs to limit Dox-induced cardiotoxicity in mESCs-derived cardiac cells, as in vitro model cell to provide a simple direct approach for further clinical therapies. Based on bioinformatics data mining, eventually miR-130a was selected to target PPARγ. This miRNA is highly expressed in heart. The expression of miR-130a increases sharply upon Dox treatment while specific antagomiR-130a reverses Dox-induced reduced expression of PPARγ, cellular apoptosis, and inflammation. Our data strongly suggest that antagomiR-130a limits Dox-induced cellular toxicity via PPARγ upregulation and may have clinical relevance to limit in vivo Dox toxicity.

Long Non-coding RNAs (lncRNAs) refer to all non-protein coding transcripts longer than 200 nucleotides. Their critical roles in different biological pathways have been already well established. Altered expression of lncRNAs can be involved in the cancer initiation and/or progression. Since patients with hepatocellular carcinoma (HCC) are usually diagnosed in late stages, developing diagnostic methods seems to be essential. In this study, the expression levels of different lncRNAs were systematically analysed in different genomic and transcriptome datasets. The analyses showed that SNHG6 is among the lncRNAs with distinctive dysregulation of expression and copy number variation in HCC tumors compared with normal tissues. The results also suggest that the dysregulation of SNHG6 is highly cancer type specific. Through co-occurrence analyses, we found that SNHG6 and its related co-expressed genes on 8q are involved in the structural integrity of ribosome and translation. This comprehensive in silico analysis, provides a resource for investigating SNHG6 in hepatocellular carcinoma and lays the groundwork for design of next researches.

HOTAIR is an lncRNA that has been known to have an oncogenic role in different cancers. There is limited knowledge of genetic and epigenetic elements and their interactions for the gene encoding HOTAIR . Therefore, understanding the molecular mechanism and its regulation remains to be challenging. We used different in silico analyses to find genetic and epigenetic elements of HOTAIR gene to gain insight into its regulation. We reported different regulatory elements including canonical promoters, transcription start sites, CpGIs as well as epigenetic marks that are potentially involved in the regulation of HOTAIR gene expression. We identified repeat sequences and single nucleotide polymorphisms that are located within or next to the CpGIs of HOTAIR . Our analyses may help to find potential interactions between genetic and epigenetic elements of HOTAIR gene in the human tissues and show opportunities and limitations for researches on HOTAIR gene in future studies.

Metachromatic leukodystrophy disorder (MLD) is an autosomal recessive and lysosomal storage disease. The disease is caused by the deficiency of the enzyme arylsulfatase A (ARSA) which is encoded by the ARSA gene. Different mutations have been reported in different populations. The present study was aimed to detect the mutation type of the ARSA gene in three relative Iranian patients. We found a novel homozygous missense mutation c.1070 G > T (p.Gly357Val) in exon 6 of these patients. The mutation was found to be reported for the first time in MLD patients. The data can update the mutation profile and contribute toward improved clinical management and counseling of MLD patients.

Objective: Forkhead box (FOX) proteins are important regulators of the epithelial-to-mesenchymal transition (EMT), which is the main mechanism of cancer metastasis. Different studies have shown their potential involvement in progression of cancer in different tissues such as breast, ovary and colorectum. In this study, we aimed to analyze the expression of genes encoding two FOX proteins in gastric adenocarcinoma., Materials and Methods: In this experimental case-control study, the expression of FOXC2 and FOXQ1 was examined in 31 gastric adenocarcinoma tumors and 31 normal adjacent gastric tissues by reverse transcription polymerase chain reaction (PCR)., Results: The expression of both genes was significantly up-regulated in gastric adenocarcinoma tumors compared with the normal tissues (P<0.05). The differential expression of these two genes was also correlated with the grade of tumors (P<0.01)., Conclusion: We show that up-regulation of FOXC2 and FOXQ1 are likely to be involved in the progression of gastric adenocarcinoma.

Recent reports have indicated that small RNAs have key roles in the response of the E.coli to stress and also in the regulating of virulence factors. It seems that some small non-coding RNAs are involved in multidrug resistance. Previous studies have indicated that rprA can increase the tolerance to Kanamycin in RcsB-deficient Escherichia coli K-12 following osmotic shock. The current study aims to clone and over-express the non-coding RNA rprA in E.coli and investigate its effect on the bacterial resistance to Kanamycin without any osmotic shock. For this purpose, rprA gene was amplified by the PCR and then cloned into the PET-28a (+) vector. The recombinant plasmid was transformed into wild type E.coli BL21 (DE3). The over expression was induced by IPTG and confirmed by qRT-PCR. The resistance to the kanamycin was then measured in different times by spectrophotometry. The statistical analysis showed that the rprA can increase the resistance to Kanamycin in Ecoli K12. The interaction between rprA and rpoS was reviewed and analyzed by in silico methods. The results showed that the bacteria with over-expressed rprA were more resistant to Kanamycin. The present study is an important step to prove the role of non-coding RNA rprA in bacterial resistance. The data can be the basis for future works and can also help to develop and deliver next-generation antibiotics.

Different mechanisms, including transcriptional and post transcriptional processes, regulate tissue specific expression of genes. In this study, we report differences in gene/protein compositional features between apoptosis involved genes selectively expressed in human tissues. We found some correlations between codon/amino acid usage and tissue specific expression level of genes. The findings can be significant for understanding the translational selection on these features. The selection may play an important role in the differentiation of human tissues and can be considered for future studies in diagnosis of some diseases such as cancer.

Epigenetic complexes control various pathways within the cells. Their abnormalities can be involved in the initiation and the progression of different types of cancer. Nucleosome remodeling and deacetylase (NuRD) is an epigenetic complex that comprises several subunits such as PHF6. Although PHF6 is reported as a tumor suppressor in some of the hematopoietic malignancies, its function is still challenging in other cancers. Our study aimed at investigating the role of PHF6 in different types of cancer. We conducted a meta-analysis of PHF6 in human cancers at genomic, transcriptomic, and proteomic levels. For this purpose, we acquired the data from several databases, and tried to statistically integrate and analyze the data in order to find the potential role of PHF6 in different tumors. The results demonstrated that although PHF6 has been previously known as a tumor suppressor gene, it was remarkably overexpressed in many cancer types such as breast and colorectal cancers. Notably, PHF6 was under-expressed in a few types of cancer, including esophageal tumors. Moreover, the results indicated that although the mutation rate of PHF6 is relatively low, it is mutated in some tumor types.  In addition, our data for 40 epigenetic genes showed that missense and nonsense mutations were associated with overexpression and under-expression, respectively. Our results suggest that PHF6 may function as an oncogenic factor in several types of cancer. We also hypothesize that PHF6 may also play its role in a tissue-specific manner. Our findings suggest further investigations regarding the exact role of PHF6 in tumor types.

Long non-coding RNAs (lncRNAs) refer to a group of RNAs that are usually more than 200 nucleotides and are not involved in protein generation. Instead, lncRNAs are involved in different regulatory processes, such as regulation of gene expression. Different lncRNAs exist throughout the genome. LncRNAs are also known for their roles in different human diseases such as cancer. HOTAIR is an lncRNA that plays a role as an oncogenic molecule in different cancer cells, such as breast, gastric, colorectal, and cervical cancer cells. Therefore, HOTAIR expression level is a potential biomarker for diagnostic and therapeutic purposes in several cancers. This RNA takes part in epigenetic regulation of genes and plays an important role in different cellular pathways by interacting with Polycomb Repressive Complex 2 (PRC2). In this review, we describe the molecular function and regulation of HOTAIR and its role in different types of cancers.

Different mechanisms regulate the expression level of tissue specific genes in human. Here we report some compositional features such as codon usage bias, amino acid usage bias, codon frequency, and base composition which may be potentially related to mRNA amount of tissue specific tumor suppressor genes. Our findings support the possibility that structural elements in gene and protein may play an important role in the regulation of tumor suppressor genes, development, and tumorigenesis. The data presented here can open broad vistas in the understanding and treatment of a variety of human malignancies., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Different long non-coding RNAs (lncRNAs) are transcribed within the genome. Although initially argued to be spurious transcriptional noise, these RNAs play important roles in biological pathways, as shown by different studies. Also, there are some reports about the role of lncRNAs in different cancers. They can contribute to the development and progression of cancer by the functioning as oncogene or/and tumor suppressor molecules. In this review, we point to some important lncRNAs as examples which seem to be involved in cancer initiation/progression.

Polycomb Repressive Complex2 maintains a predetermined state of transcription which constitutes a cellular memory stable over many cell divisions. Since this complex acts through the regulation of chromatin structure, it is important to understand how it is recruited to chromatin. The specific target sequences of this complex such as PRE (polycomb repressive element) have not been completely recognized in human genome. In this study, we have compared the target sequences of this complex with non-target genes in tumor cell lines. Through in silico and statistical analyses, we have identified some motifs which are over-represented in target genes against non-target genes. Analyzing these motifs shows some transcription factors which are potential recruiters of Polycomb repressive complex2.

Limited understanding of the Rb1 locus hinders genetic and epigenetic analyses of Retinoblastoma, a childhood cancer of the nervous systems. In this study, we used in silico tools to investigate and review putative genetic and epigenetic elements of the Rb1 gene. We report transcription start sites, CpG islands, and regulatory moieties that are likely to influence transcriptional states of this gene. These might contribute genetic and epigenetic information modulating tissue-specific transcripts and expression levels of Rb1. The elements we identified include tandem repeats that reside within or next to CpG islands near Rb1's transcriptional start site, and that are likely to be polymorphic among individuals. Our analyses highlight the complexity of this gene and suggest opportunities and limitations for future studies of retinoblastoma, genetic counseling, and the accurate identification of patients at greater risk of developing the malignancy.

Tight junctions (TJs) of epithelia are responsible for integrity of polarized epithelial cells. It is now well established that the deregulation of their functions and expressions contribute to initiation and progression of cancer through activation of cytoskeleton machinery. The aim of this study was to examine the expression level of two genes encoding tight junction-associated proteins of Jam2 and Jam3 in gastric adenocarcinoma and compare with normal gastric tissues dissected from same patients. Significant difference of expression level for these genes was observed between tumor and adjacent normal tissues. Also, we analyzed the expression level of actin filament-associated protein gene that appears to be a downstream factor of JAM2 and JAM3. The expression level of this gene was significantly higher in tumor tissues. Some correlations between the expression level of these genes with each other and with pathological features were observed. These data brought new evidences for the role of these three genes in progression of gastric adenocarcinoma.

HOTAIR is a known long non-coding RNA which has recently been associated with the progression of some cancer types. It has been reported that HOTAIR expression is correlated with SUZ12 expression level and therefore may affect the epigenetic state of cancer tissues. Here, we found aberrant up-regulation of HOTAIR in gastric adenocarcinoma samples compared with normal adjacent gastric epithelium tissues. Besides, we found that the aberrant expression of HOTAIR was associated with TNM staging and lymph node metastasis of gastric tumors. Here, a potential cooperative expression between HOTAIR and SUZ12 genes in gastric adenocarcinoma tissues is deduced. This result suggests a role for HOTAIR long non-coding RNA in gastric cancer progression.

Codon usage bias has been observed in various organisms. In this study, the correlation between SHH genes expression in some tissues and codon usage features was analyzed by bioinformatics. We found that translational selection may act on compositional features of this set of genes.