@article{4c06dd697a7a4482b74a3b95c61ec57a,
title = "Bone marrow stromal cell-derived growth inhibitor serves as a stress sensor to induce autophagy",
abstract = "Autophagy is an evolutionarily conserved stress response that promotes the lysosomal degradation of intracellular components. The bone marrow stromal cell-derived growth inhibitor (BDGI) functions as a stress sensor which is upregulated by oxidative stress and DNA damage. However, the role of BDGI in autophagic response to certain stresses remains unknown. Here, our results demonstrate that BDGI defines the impact of autophagy induction under stresses. Overexpression of BDGI promotes, while knockdown of BDGI impairs, autophagy. Mechanistically, BDGI localizes to the nucleus and interacts with the transcription factor transcription factor EB to increase the expression of multiple autophagy- and lysosome-related genes. In addition, BDGI regulates autophagy in a p53-dependent manner. Furthermore, BDGI-induced autophagy enables cell survival under stress conditions. Taken together, our study demonstrates that BDGI is a stress sensor that positively regulates autophagy.",
keywords = "autophagy, BDGI, cell death, p53, TFEB",
author = "Jianbin Zhang and Liming Wang and Jian Xu and Yancheng Tang and Bo Huang and Zhifeng Chen and Ting Zhang and Shen, {Han Ming} and Yihua Wu and Dajing Xia",
note = "Funding Information: This work was supported by research grants from National Natural Science Foundation of China (31471297, 81773016, and 21976155) to DJX, Zhejiang Provincial Natural Science Foundation of China (LY18C060001) to YHW, and National Natural Science Foundation of China (31701199) and Zhejiang Provincial Natural Science Foundation of China (LR18H160002) to JBZ, and LMW was supported by a NUSMed Post‐Doctoral Fellowship. We would like to thank Dr. Noboru Mizushima (Tokyo Medical and Dental University, Japan) for the HeLa cells with stable expression of GFP‐LC3 and Dr. Bert Vogelstein (Johns Hopkins University, United States) for provision of an isogenic pair of HCT116 colon cancer cell lines (p53 and p53). +/+ −/− Funding Information: This work was supported by research grants from National Natural Science Foundation of China (31471297, 81773016, and 21976155) to DJX, Zhejiang Provincial Natural Science Foundation of China (LY18C060001) to YHW, and National Natural Science Foundation of China (31701199) and Zhejiang Provincial Natural Science Foundation of China (LR18H160002) to JBZ, and LMW was supported by a NUSMed Post-Doctoral Fellowship. We would like to thank Dr. Noboru Mizushima (Tokyo Medical and Dental University, Japan) for the HeLa cells with stable expression of GFP-LC3 and Dr. Bert Vogelstein (Johns Hopkins University, United States) for provision of an isogenic pair of HCT116 colon cancer cell lines (p53+/+ and p53−/−). Publisher Copyright: {\textcopyright} 2020 Federation of European Biochemical Societies",
year = "2020",
month = apr,
day = "1",
doi = "10.1002/1873-3468.13732",
language = "English",
volume = "594",
pages = "1248--1260",
journal = "FEBS Letters",
issn = "0014-5793",
publisher = "Wiley-Blackwell",
number = "8",
}
