Current Issue : October - December Volume : 2019 Issue Number : 4 Articles : 5 Articles
Multiple myeloma (MM) is a plasma cell dyscrasia characterized by bone marrow\ninfiltration of clonal plasma cells. The recent literature has clearly demonstrated clonal\nheterogeneity in terms of both the genomic and transcriptomic signature of the tumor. Of note, novel\nstudies have also highlighted the importance of the functional cross-talk between the tumor clone\nand the surrounding bone marrow milieu, as a relevant player of MM pathogenesis. These findings\nhave certainly enhanced our understanding of the underlying mechanisms supporting MM\npathogenesis and disease progression. Within the specific field of small non-coding RNA-research,\nrecent studies have provided evidence for considering microRNAs as a crucial regulator of MM\nbiology and, in this context, circulating microRNAs have been shown to potentially contribute to\nprognostic stratification of MM patients. The present review will summarize the most recent studies\nwithin the specific topic of microRNAs and circulating microRNAs in MM....
Objective: Extracellular vesicles derived from oral cancer cells, which include Exosomes\nand Oncosomes, are membranous vesicles secreted into the surrounding extracellular\nenvironment. These extracellular vesicles can regulate and modulate oral squamous cell carcinoma\n(OSCC) progression through the horizontal transfer of bioactive molecules including proteins,\nlipids and microRNA (miRNA). The primary objective of this study was to examine the potential to\nisolate and evaluate extracellular vesicles (including exosomes) from various oral cancer cell lines\nand to explore potential differences in miRNA content. Methods: The OSCC cell lines SCC9, SCC25\nand CAL27 were cultured in DMEM containing 10% exosome-free fetal bovine serum. Cell-culture\nconditioned media was collected for exosome and extracellular vesicle isolation after 72 hours.\nIsolation was completed using the Total Exosome Isolation reagent (Invitrogen) and extracellular\nvesicle RNA was purified using the Total Exosome RNA isolation kit (Invitrogen). Extracellular\nvesicle miRNA content was evaluated using primers specific for miR-16, -21, -133a and -155.\nResults: Extracellular vesicles were successfully isolated from all three OSCC cell lines and total\nextracellular vesicle RNA was isolated. Molecular screening using primers specific for several\nmiRNA revealed differential baseline expression among the different cell lines. The addition of\nmelatonin significantly reduced the expression of miR-155 in all of the OSCC extracellular vesicles.\nHowever, miR-21 was significantly increased in each of the three OSCC isolates. No significant\nchanges in miR-133a expression were observed under melatonin administration. Conclusions:\nAlthough many studies have documented changes in gene expression among various cancers\nunder melatonin administration, few studies have evaluated these effects on microRNAs. These\nresults may be among the first to evaluate the effects of melatonin on microRNA expression in oral\ncancers, which suggests the differential modulation of specific microRNAs, such as miR-21,\nmiR-133a and miR-155, may be of significant importance when evaluating the mechanisms and\npathways involved in melatonin-associated anti-tumor effects....
Angiogenesis plays a key role in the development and progression of lung cancer. Recent studies have found that tumor cells can\nstimulate angiogenesis by secreting exosomes, which containmany long noncoding RNAs (lncRNAs), some of which are important\nfor the development of lung cancer. However, the roles and mechanisms of exosomal lncRNAs in lung cancer angiogenesis\nhave not yet been reported. In this study, lung cancer in mice was induced by urethane; we found that growth arrest specific 5\n(GAS5) was lowly expressed in the serum exosomes and lung cancer tissues of mice with lung cancer. And there was a significant\npositive correlation between GAS5 expression in serumexosomes and lung cancer tissues. Furthermore,GAS5 was lowly expressed\nin human lung cancer tissues, lung cancer cells, and cells culture supernatant exosomes. The exosomes of lung cancer cells\npromoted human umbilical vein endothelial cells (HUVECs) proliferation and tube formation and inhibited their apoptosis. GAS5\noverexpression in lung cancer cells increased GAS5 level in cell culture supernatant exosomes. And the exosomes of lung cancer\ncells containing highGAS5 level inhibitedHUVECs proliferation and tube formation and increased their apoptosis. In addition, we\nfound that GAS5 competitively bound miRNA-29-3p with phosphatase and tensin homolog (PTEN), upregulating PTEN mRNA\nand protein expression, and inhibited level of phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PI3K) and\nserine/threonine kinase 1 (AKT) phosphorylation in HUVECs. Overall, our results suggest that exosomal GAS5 could be a new\ntherapeutic target for lung cancer which inhibits angiogenesis....
Overexpression of oncogenes and cross-talks of the oncoproteins-regulated signaling\ncascades with other intracellular pathways in breast cancer could lead to massive abnormal\nsignaling with the consequence of tumorigenesis. The ability to identify the genes having vital roles\nin cancer development would give a promising therapeutics strategy in combating the disease.\nGenetic manipulations through siRNAs targeting the complementary sequence of the oncogenic\nmRNA in breast cancer is one of the promising approaches that can be harnessed to develop more\nefficient treatments for breast cancer. In this review, we highlighted the effects of major signaling\npathways stimulated by oncogene products on breast tumorigenesis and discussed the potential\ntherapeutic strategies for targeted delivery of siRNAs with nanoparticles in suppressing the\nstimulated signaling pathways....
Genetic polymorphisms in DNA repair genesmay affect DNA repair efficiency andmay contribute to the risk of developing cancer.\nThe aim of our study was to investigate single nucleotide polymorphisms (SNPs) in RAD51 (rs2619679, rs2928140, and rs5030789)\nand XRCC3 (rs1799796) involved in DNA double-strand break repair and their relationship to prostate cancer.The study group\nincluded 99men diagnosed with prostate cancer and 205 cancer-free controls. SNP genotyping was performed using the PCR-RFLP\nmethod. A significant association was detected between RAD51 rs5030789 polymorphism and XRCC3 rs1799796 polymorphism\nand an increased risk of prostate cancer. Our results indicate that RAD51 and XRCC3 polymorphism may contribute to prostate\ncancer....
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