LARP1 knockdown inhibits cultured gastric carcinoma cell cycle progression and metastatic behavior

碘化丙啶 细胞周期 PI3K/AKT/mTOR通路 基因敲除 分子生物学 细胞凋亡 细胞生长 转染 癌症研究 膜联蛋白 化学 生物 细胞培养 程序性细胞死亡 流式细胞术 生物化学 遗传学
作者
Xin Liu,Weiming Zhang,Nuo Meng,Lianjie Lin,Guodu Tang
出处
期刊:Central European Journal of Biology [De Gruyter]
卷期号:19 (1) 被引量:1
标识
DOI:10.1515/biol-2022-0806
摘要

Abstract This study aimed to clarify the role of la-related protein 1 (LARP1) in cell cycle progression and metastatic behavior of cultured gastric carcinoma (GC) cells. To do that, LARP1 expression was detected in clinical GC tissues and cell lines using quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting. The cell viability, apoptosis, cell cycle, migration, invasion, and cell growth were examined using a Cell Counting Kit-8, Annexin V-FITC staining, propidium iodide staining, Transwell migration and invasion assays, and colony formation assays after LARP1 knockdown. Phosphatidyl inositol 3-kinase (PI3K) and AKT1 mRNA and protein expression levels of PI3K, p-AKT1, AKT1, p-BAD, p-mTOR, and p21 in si-LARP1 transfected GC cells were determined using qRT-PCR and western blotting. Here, we've shown that LARP1 expression was upregulated in human GC tissues and KATO III cells. LARP1 knockdown inhibited GC cell proliferation, cell cycle progression, migration, invasion, and colony formation and promoted apoptosis. In si-LARP1-transfected KATO III cells, the mRNA expression levels of PI3K and AKT1, PI3K protein expression, and the p-AKT1/AKT1 ratio were significantly suppressed. p-mTOR and p-BAD were significantly decreased, whereas p21 was significantly increased in si-LARP1-transfected KATO III cells. In conclusion LARP1 knockdown induces apoptosis and inhibits cell cycle progression and metastatic behavior via PI3K/AKT1 signaling in GC cells.

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