@article{a182f4940fe249d8b14302c3b09bf8d5,
title = "NUPR1 maintains autolysosomal efflux by activating SNAP25 transcription in cancer cells",
abstract = "In the advanced stages of cancer, autophagy is thought to promote tumor progression through its ability to mitigate various cellular stresses. However, the details of how autophagy is homeostatically regulated in such tumors are unknown. Here, we report that NUPR1 (nuclear protein 1, transcriptional regulator), a transcriptional coregulator, is aberrantly expressed in a subset of cancer cells and predicts low overall survival rates for lung cancer patients. NUPR1 regulates the late stages of autolysosome processing through the induction of the SNARE protein SNAP25, which forms a complex with the lysosomal SNARE-associated protein VAMP8. NUPR1 depletion deregulates autophagic flux and impairs autolysosomal clearance, inducing massive cytoplasmic vacuolization and premature senescence in vitro and tumor suppression in vivo. Collectively, our data show that NUPR1 is a potent regulator of autolysosomal dynamics and is required for the progression of some epithelial cancers.",
keywords = "NUPR1, SNAP25, autolysosomal efflux, premature senescence, transcriptional regulator",
author = "Yanchao Mu and Xiaojie Yan and Ding Li and Dan Zhao and Lingling Wang and Xiaoyang Wang and Dan Gao and Jie Yang and Hua Zhang and Yanzhe Li and Yanan Sun and Yiliang Wei and Zhenfa Zhang and Xinzhong Chang and Zhi Yao and Shanshan Tian and Kai Zhang and Terada, {Lance S.} and Zhenyi Ma and Zhe Liu",
note = "Funding Information: This work was supported by the National Natural Science Foundation of China under grants [31371295, 81372307, 81401884, 91519331, 81773034 and 81572271], the Tianjin Municipal Science and Technology Commission under grant [13JCQNJC11300 and 16JCYBJC24500], the Specialized Research Fund for the Doctoral Program of Higher Education of China under grant [20131202120014], the High Technology Research and Development Program of China under grant [2012AA020206], HHS | National Institutes of Health (NIH) [R01CA208620] and Cancer Prevention and Research Institute of Texas (CPRIT) [RP160307]. Funding Information: This work was supported by the National Natural Science Foundation of China under grants [31371295, 81372307, 81401884, 91519331, 81773034 and 81572271], the Tianjin Municipal Science and Technology Commission under grant [13JCQNJC11300 and 16JCYBJC24500], the Specialized Research Fund for the Doctoral Program of Higher Education of China under grant [20131202120014], the High Technology Research and Development Program of China under grant [2012AA020206], HHS | National Institutes of Health (NIH) [R01CA208620] and Cancer Prevention and Research Institute of Texas (CPRIT) [RP160307]. We thank Drs. Chenghao Xuan and Lei Shi (Tianjin Medical University, Tianjin, China) for helpful discussions and critical reading of the manuscript. Publisher Copyright: {\textcopyright} 2018 Informa UK Limited, trading as Taylor & Francis Group.",
year = "2018",
month = apr,
day = "3",
doi = "10.1080/15548627.2017.1338556",
language = "English (US)",
volume = "14",
pages = "654--670",
journal = "Autophagy",
issn = "1554-8627",
publisher = "Landes Bioscience",
number = "4",
}