@article { author = {Rezaeigazik, Maryam and Nabiuni, Mohammad and Jalali, Hanieh and Kabuli, Majid}, title = {Investigating the Effects of Morphine on Survival and Sensitivity to Cisplatin in Ovarian Cancer Cells}, journal = {Journal of Cell and Molecular Research}, volume = {11}, number = {1}, pages = {1-7}, year = {2019}, publisher = {Ferdowsi University of Mashhad}, issn = {2008-9147}, eissn = {2717-3364}, doi = {10.22067/jcmr.v11i1.78768}, abstract = {Morphine as an analgesic drug is used frequently in cancer patients. Contradictory results have been achieved from previous studies related to morphine effects in different concentrations. In current study, we examined the effect of clinical concentrations of morphine on A2780Cp cell line related to ovarian cancer. Moreover, its effect on the cytotoxicity of cisplatin was investigated. A2780CP cells were cultured in RPMI1640 medium and treated with clinical doses of morphine alone or in combination with cisplatin. The rate of cell proliferation was measured using MTT assay, morphological changes of nuclei were revealed by 4′,6-diamidino-2-phenylindole (DAPI) staining, and expression of B-cell lymphoma 2 (Bcl-2) was measured using flowcytometry. MTT assay results showed clinical concentration of morphine had no effect on viability of A2780CP cells and toxicity of cisplatin. DAPI staining revealed no chromatin condensation in presence of morphine, and flowcytometry analysis showed that the expression of Bcl-2 in treated cells did not differ from control cells. In accordance with findings in other kinds of cancer, our results demonstrated that morphine did not interact with the function of cispatin in ovarian cancer. This finding can be considered in clinical applications of morphine.}, keywords = {morphine,ovarian cancer,Apoptosis,cytotoxicity,cisplatin}, url = {https://jcmr.um.ac.ir/article_29629.html}, eprint = {https://jcmr.um.ac.ir/article_29629_08328ddce6f3acfc3aae69210176e6de.pdf} } @article { author = {Mirzadeh azad, Fatemeh and Malakootian, Mahshid and Mowla, Seyed Javad}, title = {The Regulatory Effect of lncRNA PSORS1C3 on Different Variants of OCT4 in non-Pluripotent Cells}, journal = {Journal of Cell and Molecular Research}, volume = {11}, number = {1}, pages = {8-13}, year = {2019}, publisher = {Ferdowsi University of Mashhad}, issn = {2008-9147}, eissn = {2717-3364}, doi = {10.22067/jcmr.v11i1.79988}, abstract = {OCT4 is the major regulator of pluripotency in embryonic stem cells and its association with tumorigenesis, cellular stress response, and homeostatic multifactorial diseases have been recently reported. To serve the versatility in its function, OCT4 generates several transcript variants which their expression levels are tightly regulated through different mechanisms. PSORS1C3 is a long non-coding RNA with overlapping genomic location with OCT4 gene. Here, we investigated the effect of PSORS1C3 overexpression on OCT4 expression in different cell lines. Our data revealed that ectopic expression of PSORS1C3 did not affect OCT4 transcripts abundance in NT2 cells, as a model of pluripotent cells. However, in HEK293T cells, PSORS1C3 overexpression led to an increase in OCT4B as a homeostatic isoform and a decrease in OCT4A transcript level. We also observed that manipulating PSORS1C3 in HeLa cells, as a model of epithelial carcinoma line, caused an upregulation in OCT4A, OCT4C which could regulate stemness and proliferation and OCT4B transcripts at different time points. Our findings indicated that PSORS1C3 could affect the expression level of OCT4 spliced variants, according to their functions and the cells molecular context as well as genetic background. Considering these diverse regulatory effects and co-expression of OCT4 and PSORS1C3 in some cell lines, it is safe to consider PSORS1C3 as a modulator of OCT4 expression in non-pluripotent cells and in association with homeostatic pathways.}, keywords = {OCT4,PSORS1C3,expression regulation,lncRNA}, url = {https://jcmr.um.ac.ir/article_29653.html}, eprint = {https://jcmr.um.ac.ir/article_29653_6d4135f4fa645ed3e82c0239ea411dda.pdf} } @article { author = {Ashrafi, Fereshteh and Nassiri, Mohammadreza and Rezaee, Seyed Abdolrahim and Javadmanesh, Ali}, title = {The Comparative Analysis of Gene Expression Profiles in Lymph Node Cells of Naturally BLV-infected and Uninfected Bovine}, journal = {Journal of Cell and Molecular Research}, volume = {11}, number = {1}, pages = {14-22}, year = {2019}, publisher = {Ferdowsi University of Mashhad}, issn = {2008-9147}, eissn = {2717-3364}, doi = {10.22067/jcmr.v11i1.82582}, abstract = {Bovine leukemia virus (BLV) is the etiologic agent of enzootic bovine leucosis (EBL) for the bovine host. In this study to examine gene expression changes in the manifestation of the EBL malignancy, four pooled RNA samples (three RNAs in each sample) were applied for transcriptome sequencing using RNA-seq technique. Differential expression analysis was done to compare the infected bovine group with the healthy bovine group using DESeq2 package in R software. Furthermore, functional gene ontology (GO) term and KEGG pathway enrichment analysis were stablished using the DAVID online database to identify involved GO terms and pathways in the host response to BLV infection. Our results suggested that 371 up- and 72 downregulated genes were involved in EBL with statistically significant threshold log2foldchange (LFC) = 1 and false discovery rate (FDR) <0.05 that were enriched in 74 biological processes and 20 KEGG pathways. Most of identified genes were associated with cancer, especially B-cell malignancies. The glycolysis/glycogenesis metabolic process is activated in B cells that confers growth and survival advantages in tumor and dysregulated CXCL10, IL17R, BTK, CDK4 and SYK genes known as valid biomarkers to increase the proliferation of malignant cell. The outcomes can provide a list of involved genes in the malignancy and help to screen candidate genes for cancer therapy in the future.}, keywords = {BLV,EBL,transcriptome,RNA-seq,Gene Ontology}, url = {https://jcmr.um.ac.ir/article_29684.html}, eprint = {https://jcmr.um.ac.ir/article_29684_fbf30b2ad73a100fc358a53dd5ac0660.pdf} } @article { author = {Hosseinzadeh Colagar, Abasalt and Salehi-Doon, Masomeh}, title = {The LEPR (853A>G and 511A>G) Transitions may Enhance Idiopathic Recurrent Miscarriage: Evidences Based on Case-control and in silico Studies}, journal = {Journal of Cell and Molecular Research}, volume = {11}, number = {1}, pages = {23-36}, year = {2019}, publisher = {Ferdowsi University of Mashhad}, issn = {2008-9147}, eissn = {2717-3364}, doi = {10.22067/jcmr.v11i1.81426}, abstract = {Previous studies in human leptin receptor protein (LEPR) signaling are important in the establishment of fetal growth. Idiopathic recurrent miscarriage (IRM) may be the result of abnormal placental and fetal development. Thus single nucleotide polymorphisms (SNPs) of LEPR might be associated with IRM. In our case-control study, which conducted from 2017 to 2018 at the Milad Sari Genetic Detection Center and Razi Hospital (Ghaemshahr, Iran), 140 samples, including 70 cases with history of three or more IRM as before the 22nd week of gestation, and 70 controls with at least two live births and no history of pathologic pregnancies during reproductive period were studied. Polymorphisms of maternal LEPR 853A>G and 511A>G were assessed by PCR-RFLP and SSCP, respectively. Results showed that 853A>G SNP, contained frequent genotype AG (p= 0.002; OR= 0.391; 95% CI= 0.154-0.664) and G allele (p= 0.003; OR= 0.125; 95% CI= 0.032–0.489), revealed a significant protective association with IRM. Primary screening of 511A>G showed that 63 case-samples were AG genotype. PCR directed sequence showed this SNP contained frequent genotype for AG (p= 0.001; OR= 0.57; 95% CI= 0.22-0.147) and G allele (p= 0.006; OR= 0.34; 95% CI= 0.008–0.149), revealed a significant protective association with IRM. Based on our findings, LEPR (853A>G and 511A>G) gene transitions not only might enhance IRM but also could be useful genetic markers in susceptibility and severity of recurrent miscarriage.}, keywords = {LEPR gene,obesity,recurrent miscarriage}, url = {https://jcmr.um.ac.ir/article_29723.html}, eprint = {https://jcmr.um.ac.ir/article_29723_c1d6618e13c5c1a467613113d27a7ab4.pdf} } @article { author = {Momeni-Moghaddam, Madjid}, title = {EZH2 Gene Silencing Can Affect the Expression of miR-155 and TP53INP1}, journal = {Journal of Cell and Molecular Research}, volume = {11}, number = {1}, pages = {37-41}, year = {2019}, publisher = {Ferdowsi University of Mashhad}, issn = {2008-9147}, eissn = {2717-3364}, doi = {10.22067/jcmr.v11i1.82685}, abstract = {Many genetic, epigenetic, and cellular studies on cancer are underway today, and the completion of the genetic and epigenetic library of cancer could be the way to treat the disease in the future. In this study, we have investigated the parallel gene expression changes of EZH2 and miR-155. So far no study has examined the role of these two factors simultaneously and the results of this study could be useful for further studies. For this purpose, using specific shRNA, the EZH2 gene of HCT116 cells was downregulated and then the changes in expression of the miR-155 were investigated. For gene expression study, Real-time PCR as a standard quantitative method was used. The findings of this study showed that in HCT116 human colon cancer cells, downregulation of miR-155 using shRNA can reduce EZH2 expression and also can promote a significant increase in the expression of TP53INP1 gene. Based on the results, we can emphasize the interaction between these two genes. Importantly, EZH2 downregulation has been able to decrease the amount of miR-155 that has also increased expression in many types of cancers. It may be of interest in epigenetic treatments of colon cancer, because miR-155 can control a very important tumor suppressor gene, TP53INP1.}, keywords = {1,colorectal cancer,EZH2,miR-155,epigenetic,HCT116 cell line}, url = {https://jcmr.um.ac.ir/article_29755.html}, eprint = {https://jcmr.um.ac.ir/article_29755_0302afbd46dce14a60efc3e4cc85c9a4.pdf} }