microRNA-630 promotes cell proliferation and inhibits apoptosis in the HCT116 human colorectal cancer cell line

Abstract

Dysregulation of microRNAs (miRNAs) in colorectal cancer provides important opportunities for the development of future miRNA‑based therapies. The present study aimed to assess the role of miRNA‑630 (miR‑630) expression in colorectal cancer. HCT116 human colorectal cancer cells were transfected with miR‑630 inhibitor, mimic or control miRNA, and the effects of miR‑630 dysregulation on cell viability, proliferation and apoptosis were analyzed using MTT and bromodeoxyuridine assays, and an annexin V‑fluorescein isothiocyanate cell apoptosis kit, respectively. In addition, the changes in the protein expression of proliferation‑associated and AKT signaling pathway proteins were analyzed by western blot analysis. The results of the present study demonstrated that overexpression of miR‑630 significantly promoted HCT116 cell proliferation however inhibited apoptosis. Furthermore, miR‑630 overexpression reduced the protein expression of p27, BCL2‑associated X apoptosis regulator, procaspase‑3 and active caspase‑3, and increased the levels of phosphorylated‑AKT and BCL2 apoptosis regulator. The suppression of miR‑630 led to the opposite results. In conclusion, the present findings suggested that miR‑630 may function as an oncogenic miRNA in colorectal cancer, and may promote cellular proliferation and inhibit apoptosis, through the regulation of the expression of p27 and the AKT signaling pathway. The present study suggested that the inhibition of miR‑630 may have potential as an alternative therapeutic strategy for the treatment of patients with colorectal cancer.

MiR-10b alleviates high glucose-induced human retinal endothelial cell injury by regulating TIAM1 signaling

“…Most mature miRNAs precisely regulate target genes by binding to the 3'untranslated region (UTR) of their mRNAs [7]. Compelling evidence has indicated that miRNAs play vital roles in many biological processes, including tumorigenesis, apoptosis, proliferation, and cell differentiation [8][9][10]. For example, miRNA-1273g-3p and miRNA-451a have been shown to play vital roles in the regulation of DR; thus, they may serve as new targets for DR treatment [11,12].…”

Circular RNA MTO1 intercorrelates with microRNA‐630, both associate with Enneking stage and/or pathological fracture as well as prognosis in osteosarcoma patients

“… 19 In our study, we found that: (1) miR‐630 expression in tumor tissue was higher than that in non‐tumor tissue, a possible explanation might that: miR‐630 reflected the proliferation rate of cells, and meanwhile, the proliferation rate in osteosarcoma cells was higher than that in the adjacent tissue cells. Therefore, miR‐630 expression was higher in tumor tissue than in non‐tumor tissue; (2) elevated miR‐630 was correlated with the occurrence of pathological fracture and deteriorated disease severity feature, the reason might be that: elevated miR‐630 promoted malignant osteosarcoma cell proliferation, 21 which might contribute to the osteosarcoma progression, subsequently causing bone lesion and deteriorated disease feature 6 ; (3) elevated miR‐630 expression was associated with poor neoadjuvant treatment response, the explanations could be that: miR‐630 expression might increase cisplatin resistance in osteosarcoma, 22 thus causing unfavorable treatment response; (4) miR‐630 high was associated with shorter DFS, a possible reason could be that: its association with deteriorated disease feature and unfavorable treatment response (as above mentioned) might indirectly resulted in poor DFS.…”

“…(2) elevated miR-630 was correlated with the occurrence of pathological fracture and deteriorated disease severity feature, the reason might be that: elevated miR-630 promoted malignant osteosarcoma cell proliferation, 21…”

Overexpression of microRNA‑936 suppresses non‑small cell lung cancer cell proliferation and invasion via targeting E2F2

“…miRs have been reported to serve as oncogenes or tumor suppressors to regulate cancer cell proliferation and migration. For instance, Zhang et al (26) reported that miR-630 promotes cell proliferation and inhibits apoptosis in the HCT116 human colorectal cancer cell line. Furthermore, Liu et al (27) revealed that miR-1297 contributes to tumor growth of human breast cancer by targeting PTEN/ phosphoinositide 3-kinase/AKT signaling.…”