microRNA-3129 promotes cell proliferation in gastric cancer cell line SGC7901 via positive regulation of pRb

Abstract

Several microRNAs (miRNAs) have been reported as oncogenes or tumor suppressors in many cancers, including gastric cancer (GC). However, the role and molecular mechanism of miR-3129 in GC is largely unknown. We aimed to explore the function and the underlying molecular mechanism of miR-3129 in GC. Cancer tissues and corresponding adjacent tissues were collected from 50 patients with GC, and the expression of miR-3129 was detected by RT-qPCR. The expression of miR-3129 and pRb in human GC cell line SCG7091 was altered by transient transfection. Thereafter, MTT and flow cytometry assays were used to analyze cell viability and cell cycle. The expression of cyclin E, CDK2, CDK2 inhibitors (p16 and 21), and pRb were detected by RT-qPCR and western blot. A significant up-regulation of miR-3129 was observed in GC tissues compared to adjacent tissues. Overexpression of miR-3129 significantly improved cell viability after 4 days of post-transfection. Flow cytometry assay results showed that the miR-3129 overexpression arrested more SGC7901 cells at S phase. Moreover, overexpression of miR-3129 down-regulated the expression of CDK2 inhibitors while it up-regulated the expression levels of cyclin E, CDK2, and pRb. Interestingly, we found that pRb inhibition reversed the effect of miR-3129 inhibitor on cell proliferation in SGC7901 cells, increased cell viability, reduced cells at G0/1 phase, and modulated the expression of proliferation-related factors. Our results revealed that miR-3129 functioned as an oncogene through positive regulation of pRb and may prove to be a promising option for molecular therapy of GC.

RETRACTION: miR-384 targets metadherin gene to suppress growth, migration, and invasion of gastric cancer cells

“…GC is prevalent in East Asia, especially in China. 15 Various miRNAs have been suggested to play important tumor suppressor or oncogenic roles in GC, 8,9 although the mechanisms whereby miRNAs impact the behaviors of GC cells remain unclear. Furthermore, miR-384 has been reported to function as a tumor suppressor in multiple human cancers, but its function in GC has not previously been examined.…”

“…Previous studies suggested that miRNAs act by regulating downstream tumor-associated genes. 8–13 It is therefore necessary to investigate the targets of miR-384 in GC to determine the mechanisms underlying its role in the progression of GC. Using mechanistic assays (luciferase reporter assay and western blot), we demonstrated that MTDH was a direct target of miR-384.…”

miR-204-5p Suppress Lymph Node Metastasis via Regulating CXCL12 and CXCR4 in Gastric Cancer

“…Currently, accumulating evidence demonstrated that microRNAs (miRNAs), as a class of endogenous noncoding short RNA serve as oncogenes and onco-suppressors in diverse human carcinogenesis including GC [6][7][8][9]. Many of them are associated with crucial biological processes, such as cell proliferation, metastasis, and invasion, by regulating relevant targets gene expression at post-transcriptional levels.…”

Elevated serum miR‐3129‐5p contributes to the progression of coronary heart disease via targeting mTOR

“…The oncogenic role of miR-3129-5p is found in various cancers, including epithelial ovarian cancer and gastric cancer. 22,23 Interestingly, adipocyte-derived extracellular vesicle miR-3129-5p is reported to increase macrophage cholesterol efflux capacity, which may be a predictor for cardiovascular disease. 24 Here, we found that the relative expression of miR-3129-5p was found to be gradually elevated with the increase in Gensini score, indicating that the expression of miR-3129-5p correlated with the increase in coronary atherosclerosis.…”

“…The oncogenic role of miR‐3129‐5p is found in various cancers, including epithelial ovarian cancer and gastric cancer 22,23 . Interestingly, adipocyte‐derived extracellular vesicle miR‐3129‐5p is reported to increase macrophage cholesterol efflux capacity, which may be a predictor for cardiovascular disease 24 .…”