RSK2 protects human breast cancer cells under endoplasmic reticulum stress through activating AMPKα2-mediated autophagy View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2020-09-21

AUTHORS

Lan-Ya Li, Xi-Sha Chen, Kuan-Song Wang, Yi-Di Guan, Xing-Cong Ren, Dong-Sheng Cao, Xin-Yuan Sun, Ao-Xue Li, Yong-Guang Tao, Yi Zhang, Ming-Zhu Yin, Xin-Luan Wang, Ming-Hua Wu, Jin-Ming Yang, Yan Cheng

ABSTRACT

Autophagy can protect stressed cancer cell by degradation of damaged proteins and organelles. However, the regulatory mechanisms behind this cellular process remain incompletely understood. Here, we demonstrate that RSK2 (p90 ribosomal S6 kinase 2) plays a critical role in ER stress-induced autophagy in breast cancer cells. We demonstrated that the promotive effect of RSK2 on autophagy resulted from directly binding of AMPKα2 in nucleus and phosphorylating it at Thr172 residue. IRE1α, an ER membrane-associated protein mediating unfolded protein response (UPR), is required for transducing the signal for activation of ERK1/2-RSK2 under ER stress. Suppression of autophagy by knockdown of RSK2 enhanced the sensitivity of breast cancer cells to ER stress both in vitro and in vivo. Furthermore, we demonstrated that inhibition of RSK2-mediated autophagy rendered breast cancer cells more sensitive to paclitaxel, a chemotherapeutic agent that induces ER stress-mediated cell death. This study identifies RSK2 as a novel controller of autophagy in tumor cells and suggests that targeting RSK2 can be exploited as an approach to reinforce the efficacy of ER stress-inducing agents against cancer. More... »

PAGES

6704-6718

References to SciGraph publications

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  • Journal

    TITLE

    Oncogene

    ISSUE

    43

    VOLUME

    39

    Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41388-020-01447-0

    DOI

    http://dx.doi.org/10.1038/s41388-020-01447-0

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1131004394

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/32958832


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