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BHLHE41 通过 MAPK/JNK 通路抑制 MCF-7 细胞侵袭。

BHLHE41 suppresses MCF-7 cell invasion via MAPK/JNK pathway.

机构信息

Department of Pathology, The First Affiliated Hospital, China Medical University, Shenyang, China.

Department of Pathology, College of Basic Medical Sciences, China Medical University, Shenyang, China.

出版信息

J Cell Mol Med. 2020 Apr;24(7):4001-4010. doi: 10.1111/jcmm.15033. Epub 2020 Feb 19.

DOI:10.1111/jcmm.15033
PMID:32073238
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7171311/
Abstract

Deregulation of the basic helix-loop-helix family member e41 (BHLHE41) has been characterized as a marker of progression of several cancers. In this study, we aimed to explore the mechanism by which BHLHE41 regulates the invasion of breast cancer cells. BHLHE41 suppresses, whereas the silencing of BHLHE41 promotes tumour invasion of both MCF-7 and MDA-MB-231 cells. Meanwhile, BHLHE41 down-regulated the transcription and translation of SNAI1, SNAI2, VIM and CDH2, and up-regulated those of CLDN1, CLDN4 and CDH1. Reporter assay indicated that silencing of BHLHE41 dramatically activated the MAPK/JNK signalling pathway in MCF-7 cell line and the hypoxia signalling pathway in MDA-MB-231 cell line. Furthermore, silencing of BHLHE41 activated the MAPK/JNK signalling pathway by up-regulating phosphorylated JNK and failed to affect the expression of HIF-1 alpha in MCF-7 cells. After blocking the MAPK/JNK signalling pathway by specific inhibitor SP600125, silencing of BHLHE41 failed to promote tumour cell invasion. These results suggest that BHLHE41 facilitates MCF-7 cell invasion mainly via the activation of MAPK/JNK signalling pathway. In conclusion, although BHLHE41 suppresses tumour invasion in MCF-7 and MDA-MB-231 cell lines, the specific regulatory mechanisms may be different.

摘要

BHLHE41 是碱性螺旋-环-螺旋家族成员之一，其失调已被证实是多种癌症进展的一个标志。在本研究中，我们旨在探讨 BHLHE41 调节乳腺癌细胞侵袭的机制。BHLHE41 抑制 MCF-7 和 MDA-MB-231 细胞的肿瘤侵袭，而 BHLHE41 的沉默则促进了这一过程。同时，BHLHE41 下调 SNAI1、SNAI2、VIM 和 CDH2 的转录和翻译，上调 CLDN1、CLDN4 和 CDH1 的转录和翻译。报告基因检测表明，BHLHE41 的沉默在 MCF-7 细胞系中显著激活了 MAPK/JNK 信号通路，在 MDA-MB-231 细胞系中激活了低氧信号通路。此外，BHLHE41 的沉默通过上调磷酸化 JNK 激活了 MAPK/JNK 信号通路，而对 MCF-7 细胞中 HIF-1α的表达没有影响。用特定的 MAPK/JNK 信号通路抑制剂 SP600125 阻断 MAPK/JNK 信号通路后，BHLHE41 的沉默未能促进肿瘤细胞侵袭。这些结果表明，BHLHE41 主要通过激活 MAPK/JNK 信号通路促进 MCF-7 细胞侵袭。总之，尽管 BHLHE41 抑制 MCF-7 和 MDA-MB-231 细胞系中的肿瘤侵袭，但具体的调控机制可能不同。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a285/7171311/84c94de64fc9/JCMM-24-4001-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a285/7171311/04e52f16c6b7/JCMM-24-4001-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a285/7171311/0b863bb96950/JCMM-24-4001-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a285/7171311/4db5402c5631/JCMM-24-4001-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a285/7171311/b9a61d6c0f0f/JCMM-24-4001-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a285/7171311/84c94de64fc9/JCMM-24-4001-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a285/7171311/04e52f16c6b7/JCMM-24-4001-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a285/7171311/0b863bb96950/JCMM-24-4001-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a285/7171311/4db5402c5631/JCMM-24-4001-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a285/7171311/b9a61d6c0f0f/JCMM-24-4001-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a285/7171311/84c94de64fc9/JCMM-24-4001-g005.jpg

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