自噬
PI3K/AKT/mTOR通路
细胞凋亡
细胞生物学
癌症研究
细胞生长
蛋白激酶B
肝细胞癌
化学
信号转导
生物
癌细胞
生物化学
作者
Tuan Tuan Hao,Rui Liao,Dengliang Lei,Gangli Hu,Fang Luo
标识
DOI:10.1016/j.intimp.2020.106889
摘要
B7-H4 and autophagy can regulate or be induced by the PI3K signaling pathway. However, the association between B7-H4 and autophagy in hepatocellular carcinoma (HCC) remains unclear. The aim of this work was to investigate whether B7-H4 regulates autophagy via the PI3K signaling pathway in HCC cells. Here, western blotting was used to measure the expression of the related proteins involved in changes in of autophagy and apoptosis, such as LC3, P62, cleaved caspase 3, cleaved PARP, BCL-2, and BAX in Huh7 and Hep3B cells. Additionally, PI3K/AKT/mTOR signaling pathway proteins were measured. Cell counting kit-8 and flow cytometry were used to analyze the effects of B7-H4 siRNA interference on cell proliferation with the interference of B7-H4 siRNA. We found that B7-H4 siRNA increased HCC cell apoptosis and autophagy, and reduced cell proliferation. Moreover, the apoptosis-related proteins cleaved caspase 3, cleaved PARP and BAX were increased and Bcl-2 was decreased after B7-H4 siRNA interference. The expression level of the autophagy-related protein LC3Ⅱ was upregulated, while expression of the autophagy adaptor P62 expression was decreased in B7-H4 siRNA-pretreated cells. Furthermore, our data revealed that B7-H4 regulated apoptosis and autophagy through the PI3K signaling pathway in HCC cells. Therefore, these results suggested that B7-H4 plays an important role in HCC progression by affecting cell apoptosis and autophagy.
科研通智能强力驱动
Strongly Powered by AbleSci AI