Pan Haiyan, Ding Yuanlin, Jiang Yugang, Wang Xingjie, Rao Jiawei, Zhang Xingshan, Yu Haibing, Hou Qinghua, Li Tao
School of Public Health, Guangdong Medical University, Dongguan, 523808, Guangdong, People's Republic of China.
Department of gastrointestinal Surgery, Shandong Provincial Hospital, Jinan, 250021, Shandong, People's Republic of China.
Cancer Cell Int. 2021 Jan 6;21(1):7. doi: 10.1186/s12935-020-01644-7.
LncRNA was known to be closely associated with the progression of human tumors. The role of lncRNA LIFR-AS1 in the pathogenesis and progression of gastric tumor is still unclear. The aim of this study was to investigate the function of LIFR-AS1 and the underlying mechanism in the pathogenesis and progression of gastric cancer.
QRT-PCR was used to evaluate the expression of LIFR-AS1, miR-29a-3p and COL1A2 in gastric tumor tissues and cells. Western blotting was used to evaluate the protein expression of COL1A2 in gastric tumor cells. CCK-8 assay, transwell assay and flow cytometry were used to evaluate the roles of LIFR-AS1, miR-29a-3p and COL1A2 in cell proliferation, invasion, migration and apoptosis. The relationship among LIFR-AS1, miR-29a-3p and COL1A2 was assessed by bioinformatics analyses and luciferase reporter assay.
The expression levels of LIFR-AS1 were significantly increased in gastric tumor tissues and cells, while the expression levels of miR-29a-3p were decreased. The expression of miR-29a-3p was negatively correlated with the expression of LIFR-AS1 in gastric cancer tumor tissues. Knocking down of LIFR-AS1 inhibited proliferation, invasion and migration of gastric tumor cells, and induced apoptosis of gastric tumor cells. Bioinformatics analyses and integrated experiments revealed that LIFR-AS1 elevated the expression of COL1A2 through sponging miR-29a-3p, which further resulted in the progression of gastric tumor.
LIFR-AS1 plays an important role as a competing endogenous RNA in gastric tumor pathogenesis and may be a potential target for the diagnosis and treatment of gastric tumor.
已知长链非编码RNA（lncRNA）与人类肿瘤的进展密切相关。lncRNA LIFR-AS1在胃肿瘤发病机制和进展中的作用仍不清楚。本研究旨在探讨LIFR-AS1在胃癌发病机制和进展中的功能及潜在机制。
采用实时定量聚合酶链反应（QRT-PCR）评估LIFR-AS1、miR-29a-3p和Ⅰ型胶原α2（COL1A2）在胃肿瘤组织和细胞中的表达。采用蛋白质免疫印迹法评估COL1A2在胃肿瘤细胞中的蛋白表达。采用细胞计数试剂盒-8（CCK-8）检测法、Transwell检测法和流式细胞术评估LIFR-AS1、miR-29a-3p和COL1A2在细胞增殖、侵袭、迁移和凋亡中的作用。通过生物信息学分析和荧光素酶报告基因检测评估LIFR-AS1、miR-29a-3p和COL1A2之间的关系。
LIFR-AS1在胃肿瘤组织和细胞中的表达水平显著升高，而miR-29a-3p的表达水平降低。在胃癌肿瘤组织中，miR-29a-3p的表达与LIFR-AS1的表达呈负相关。敲低LIFR-AS1可抑制胃肿瘤细胞的增殖、侵袭和迁移，并诱导胃肿瘤细胞凋亡。生物信息学分析和综合实验表明，LIFR-AS1通过吸附miR-29a-3p提高COL1A2的表达，进而导致胃肿瘤进展。
LIFR-AS1作为竞争性内源性RNA在胃肿瘤发病机制中起重要作用，可能是胃肿瘤诊断和治疗的潜在靶点。
