Overexpression of PIK3R1 promotes hepatocellular carcinoma progression

Biological research: BR

Lei Xiang¹  Zhi Huang²  Xuejun Ai³ 

[1] Department of Digestive, Guiyang First Peoples Hospital, Guiyang, China;Department of Interventional Radiology, Affiliated Hospital of Guizhou Medical University, Guiyang, China;The Key Laboratory of Medical Molecular Biology, Guizhou Medical University, Guiyang, China

关键词: Hepatocellular carcinoma;    PIK3R1;    Apoptosis;    Targeted therapy;   

DOI  :  10.1186/s40659-018-0202-7

学科分类：生物科学（综合）

来源: BioMed Central

【 摘 要 】

Phosphoinositide-3-kinase, regulatory subunit 1 (PIK3R1) could regulate cancer cell proliferation important for cancer cell proliferation; however, its role in Hepatocellular carcinoma (HCC) remains largely unknown. Here, we investigated the role of PIK3R1 in HCC and examined the underlying molecular mechanisms. The expression of PIK3R1 was evaluated by immunohistochemistry and qRT-PCR in a series of HCC tissues. The mRNA and protein expression of PIK3R1 was used by qRT-PCR and western blot assays in a series of human HCC cell lines, and then we choose MHCC97H and HCCLM3 cells as a model to investigate the effect of PIK3R1 on HCC progression. The effects of PIK3R1 knowdown on cell proliferation, migration, apoptosis of HCC were assessed by the MTT assay, clonogenic assays, wound healing assay and flow cytometry in vitro. Western blot assay was performed to assess the expression changes of PI3K/AKT/mTOR signaling pathway. Our results found that PIK3R1 was highly expressed in HCC tissues compared with adjacent normal tissues. Knockdown of PIK3R1 inhibited the proliferation, migration and promoted apoptosis of HCC cell lines. In addition, we proved that knockdown of PIK3R1 downregulated p-PI3K, p-AKT, and p-mTOR expressions in MHCC97H and HCCLM3 cells. In conclusion, PIK3R1 providing potential novel targets for the treatment of HCC.

【 授权许可】

CC BY