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内质网应激诱导 CAP2 表达促进肝癌细胞上皮-间充质转化。

Endoplasmic Reticulum Stress Induces CAP2 Expression Promoting Epithelial-Mesenchymal Transition in Liver Cancer Cells.

机构信息

Department of Physiology, Ajou University School of Medicine, Suwon 16499, Korea.

Department of Biomedical Science, Graduate School, Ajou University, Suwon 16499, Korea.

出版信息

Mol Cells. 2021 Aug 31;44(8):569-579. doi: 10.14348/molcells.2021.0031.

Abstract

() has been addressed as a candidate biomarker in various cancer types. Previously, we have shown that is expressed during multi-step hepatocarcinogenesis; however, its underlying mechanisms in liver cancer cells are not fully elucidated yet. Here, we demonstrated that endoplasmic reticulum (ER) stress induced expression, and which promoted migration and invasion of liver cancer cells. We also found that the ER stress-induced CAP2 expression is mediated through activation of protein kinase C epsilon (PKCε) and the promotor binding of activating transcription factor 2 (ATF2). In addition, we further demonstrated that expression promoted epithelial-mesenchymal transition (EMT) through activation of Rac1 and ERK. In conclusion, we suggest that ER stress induces expression promoting EMT in liver cancers cells. Our results shed light on the novel functions of in the metastatic process of liver cancer cells.

摘要

已经在多种癌症类型中被视为候选生物标志物。以前,我们已经表明,在多步肝癌发生过程中表达;然而,其在肝癌细胞中的潜在机制尚未完全阐明。在这里,我们证明内质网 (ER) 应激诱导 CAP2 的表达,促进肝癌细胞的迁移和侵袭。我们还发现,ER 应激诱导的 CAP2 表达是通过激活蛋白激酶 C ɛ (PKCε) 和激活转录因子 2 (ATF2) 的启动子结合来介导的。此外,我们进一步证明 CAP2 的表达通过激活 Rac1 和 ERK 促进上皮-间充质转化 (EMT)。总之,我们认为 ER 应激诱导 CAP2 的表达促进肝癌细胞的 EMT。我们的结果揭示了 CAP2 在肝癌细胞转移过程中的新功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4ab/8424138/5d2880bf2877/molce-44-8-569-f1.jpg

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