Wang Yao, Guo Zhigang, Yang Zhifeng, Deng Qingyan, Huang Yueming, Chen Yanhong
Department of Gastrointestinal Surgery, Zhongshan City People's Hospital, Zhongshan, Guangdong, 528400, P.R. China.
Department of Hospital Infection Management, Zhongshan City People's Hospital, No. 2 Sunwen East Road, Shiqi District, Zhongshan, Guangdong, 528400, P.R. China.
Open Med (Wars). 2024 Sep 27;19(1):20240992. doi: 10.1515/med-2024-0992. eCollection 2024.
The oncogenic role of long intergenic noncoding RNA for IGF2BP2 stability (LINRIS) has been reported in colorectal cancer. This research aimed to study its potential involvement in gastric cancer (GC). In this study, paired GC and non-tumor tissues were obtained from 64 GC patients, and the levels of LINRIS, mature microRNA-34a (miR-34a), and miR-34a precursor in these tissues were measured with RT-qPCR. Linear regression was used to analyze their correlations. The role of LINRIS overexpression and siRNA silencing in regulating the maturation of miR-34a was analyzed by RT-qPCR. Cell apoptosis was studied with flow cytometry. It was observed that LINRIS was overexpressed in GC and showed a negative correlation with mature miR-34a, but not miR-34a precursor. In GC cells, LINRIS siRNA silencing upregulated mature miR-34a level, but not miR-34a precursor level. LINRIS overexpression downregulated miR-34a level. Cell apoptosis analysis showed that LINRIS siRNA silencing and miR-34a overexpression promoted GC cell apoptosis and suppressed cell migration and invasion, while LINRIS overexpression suppressed cell apoptosis and enhanced cell migration and invasion. In addition, the effect of LINRIS overexpression was reversed by miR-34a overexpression. Therefore, LINRIS siRNA silencing in GC may promote cell apoptosis by promoting miR-34a maturation.
长链基因间非编码RNA对IGF2BP2稳定性的致癌作用（LINRIS）在结直肠癌中已有报道。本研究旨在探讨其在胃癌（GC）中的潜在作用。在本研究中，从64例GC患者中获取配对的GC组织和非肿瘤组织，采用RT-qPCR检测这些组织中LINRIS、成熟微小RNA-34a（miR-34a）和miR-34a前体的水平。采用线性回归分析它们之间的相关性。通过RT-qPCR分析LINRIS过表达和siRNA沉默对miR-34a成熟的调节作用。采用流式细胞术研究细胞凋亡。结果发现，LINRIS在GC中过表达，且与成熟miR-34a呈负相关，但与miR-34a前体无相关性。在GC细胞中，LINRIS siRNA沉默上调了成熟miR-34a水平，但未上调miR-34a前体水平。LINRIS过表达下调了miR-34a水平。细胞凋亡分析表明，LINRIS siRNA沉默和miR-34a过表达促进了GC细胞凋亡，抑制了细胞迁移和侵袭，而LINRIS过表达抑制了细胞凋亡，增强了细胞迁移和侵袭。此外，miR-34a过表达可逆转LINRIS过表达的作用。因此，GC中LINRIS siRNA沉默可能通过促进miR-34a成熟来促进细胞凋亡。
