Effects of miR-16 on proliferation and apoptosis of BEL-7402 hepatocellular carcinoma cells

doi:10.19401/j.cnki.1007-3639.2018.01.005

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Effects of miR-16 on proliferation and apoptosis of BEL-7402 hepatocellular carcinoma cells

更新时间：2026-01-27

- Effects of miR-16 on proliferation and apoptosis of BEL-7402 hepatocellular carcinoma cells
- China Oncology Vol. 28, Issue 1, Pages: 38-42(2018)
- 作者机构：
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- DOI：10.19401/j.cnki.1007-3639.2018.01.005
  CLC： R735.7
- Published Online：07 February 2018，
  
  Published：07 February 2018
- 稿件说明：
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缪欣,丁岚,刘浩,等.

Effects of miR-16 on proliferation and apoptosis of BEL-7402 hepatocellular carcinoma cells[J]. China Oncology, 2018, 28(1): 38-42.
缪欣,丁岚,刘浩,等. DOI： 10.19401/j.cnki.1007-3639.2018.01.005.

Effects of miR-16 on proliferation and apoptosis of BEL-7402 hepatocellular carcinoma cells[J]. China Oncology, 2018, 28(1): 38-42. DOI： 10.19401/j.cnki.1007-3639.2018.01.005.

摘要

背景与目的：miR-16和miR-15a基因复合体位于人13q14区域的DLEU2基因内含子内，是目前公认的抑癌基因之一。该基因区域的缺失与多种实体肿瘤有关，miR-16同时促进肿瘤细胞的凋亡。该研究旨在探讨miR-16对BEL-7402肝癌细胞增殖与凋亡的影响。方法：人肝癌细胞BEL-7402分为miR-16感染组(加入LV-hsamiR-16-1慢病毒)和阴性对照组(加入阴性对照病毒)，采用倒置荧光显微镜观察细胞绿色荧光的强度；采用细胞计数试剂盒(cell counting kit-8，CCK-8)检测miR-16对BEL-7402肝癌细胞增殖的影响；采用流式细胞术分析miR-16对人肝癌细胞BEL-7402的细胞周期与凋亡的影响。结果：CCK-8检测结果显示，感染组细胞增殖能力明显降低(P0.05)；流式细胞术检测结果显示，阴性对照组BEL-7402细胞周期中G

期细胞百分率数值明显下降，但S及G

/M期细胞的百分率均明显上升(P0.05)。miR-16促进BEL-7402肝癌细胞凋亡。结论：miR-16抑制BEL-7402肝癌细胞的增殖并促进其凋亡，miR-16有望成为临床肝癌靶向治疗的新靶点。

Abstract

Background and purpose: The miR-16 and miR-15a gene complexes are located within the intron of the DLEU2 gene in the human 13q14 region and are currently recognized as tumor suppressor genes. The deletion of this gene region is associated with a variety of solid tumors. miR-16 can promote tumor cell apoptosis. The purpose of this study was to investigate the effect of miR-16 on the proliferation and apoptosis of BEL-7402 hepatocarcinoma cells. Metho

ds: BEL-7402 hepatocarcinoma cells were divided into miR-16 infection group (the plasmid is expressed by the addition of the LV-hsa-miR-16-1 lentivirus) and negative control group which was infected with miR-16 lentivirus (the negative control virus CON220 was added). The intensity of green fluorescence was observed using an inverted fluorescence microscope. Cell counting kit-8 (CCK-8) was used to detect the proliferation of BEL-7402 hepatocarcinoma cells. In addition

flow cytometry was performed to detect the influence of miR-16 on cell cycle and apoptosis of BEL-7402 hepatocarcinoma cells. Results: What we found is that

compared to the negative control group

the infected cells showed an obvious decrease in the capacity of cell proliferation. The percentage of G

phase cells in the BEL-7402 cell cycle was reduced apparently

whereas the S and G

/M phase cells significantly increased (P0.05). miR-16 virus had a very significant effect on the apoptosis of BEL-7402 hepatocarcinoma cells. Conclusion: miR-16 suppresses the proliferation capacity of BEL-7402 hepatocarcinoma cells. miR-16 is expected to be a new target for targeted liver cancer therapy.

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