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紫草素通过PI3K/Akt信号通路促进BXPC-3人胰腺癌细胞的自噬。

Shikonin promotes autophagy in BXPC-3 human pancreatic cancer cells through the PI3K/Akt signaling pathway.

作者信息

Shi Shuqing, Cao Haimei

机构信息

Department of General Surgery, Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, P.R. China.

出版信息

Oncol Lett. 2014 Sep;8(3):1087-1089. doi: 10.3892/ol.2014.2293. Epub 2014 Jun 26.

Abstract

The present study aimed to investigate the effect of shikonin on autophagy in BXPC-3 human pancreatic cancer cells and its underlying mechanism. Cell viability was assessed using the Cell Counting Kit-8 assay and the expression of light chain (LC) 3, p62, phosphoinositide 3-kinase (PI3K), Akt, phosphorylated (p)-PI3K and p-Akt was analyzed using western blot analysis. Following treatment with 1 μmol/l shikonin for 48 h and 2.5 and 5 μmol/l shikonin for 24 and 48 h, the viability of the BXPC-3 cells was found to be significantly reduced and the protein expression of LC3-II/LC3-I was observed to be increased, while the protein expression of p62, PI3K, Akt, p-PI3K and p-Akt was decreased. These findings suggest that shikonin promotes autophagy in BXPC-3 cells and that the underlying mechanism may be associated with the PI3K/Akt signaling pathway.

摘要

本研究旨在探讨紫草素对人胰腺癌细胞BXPC-3自噬的影响及其潜在机制。使用细胞计数试剂盒-8法评估细胞活力,并通过蛋白质印迹分析来分析轻链(LC)3、p62、磷酸肌醇3激酶(PI3K)、Akt、磷酸化(p)-PI3K和p-Akt的表达。在用1 μmol/l紫草素处理48小时以及用2.5和5 μmol/l紫草素处理24小时和48小时后,发现BXPC-3细胞的活力显著降低,并且观察到LC3-II/LC3-I的蛋白质表达增加,而p62、PI3K、Akt、p-PI3K和p-Akt的蛋白质表达降低。这些发现表明紫草素促进BXPC-3细胞的自噬,其潜在机制可能与PI3K/Akt信号通路有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8290/4114587/1052766cc75e/OL-08-03-1087-g00.jpg

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