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

Author:

Liu Xin12,Zhang Wei-Ming3,Meng Nuo1,Lin Lian-Jie1,Tang Guo-Du1

Affiliation:

1. Department of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University , No. 6, Shuangyong Road , Nanning , Guangxi 530021 , P. R. China

2. Department of Gastroenterology, Wuming Hospital Affiliated to Guangxi Medical University , Nanning , Guangxi, 530199 , P. R. China

3. Department of Radiotherapy, Wuming Hospital Affiliated to Guangxi Medical University, Nanning , Guangxi, 530199 , P. R. China

Abstract

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.

Publisher

Walter de Gruyter GmbH

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