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Cited 8 time in webofscience Cited 8 time in scopus
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Chaperone-mediated autophagy modulates Snail protein stability: implications for breast cancer metastasisopen access

Authors
Ryu, Ki-JunLee, Ki WonPark, Seung-HoKim, TaeyoungHong, Keun-SeokKim, HyeminKim, MinjuOk, Dong WooKwon, Gu Neut BomPark, Young-JunKwon, Hyuk-KwonHwangbo, CheolKim, Kwang DongLee, J. EugeneYoo, Jiyun
Issue Date
Oct-2024
Publisher
BioMed Central
Keywords
Chaperone-mediated autophagy; Snail; EMT; Metastasis; Breast cancer
Citation
Molecular Cancer, v.23, no.1
Indexed
SCIE
SCOPUS
Journal Title
Molecular Cancer
Volume
23
Number
1
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/74476
DOI
10.1186/s12943-024-02138-0
ISSN
1476-4598
1476-4598
Abstract
Breast cancer remains a significant health concern, with triple-negative breast cancer (TNBC) being an aggressive subtype with poor prognosis. Epithelial-mesenchymal transition (EMT) is important in early-stage tumor to invasive malignancy progression. Snail, a central EMT component, is tightly regulated and may be subjected to proteasomal degradation. We report a novel proteasomal independent pathway involving chaperone-mediated autophagy (CMA) in Snail degradation, mediated via its cytosolic interaction with HSC70 and lysosomal targeting, which prevented its accumulation in luminal-type breast cancer cells. Conversely, Snail predominantly localized to the nucleus, thus evading CMA-mediated degradation in TNBC cells. Starvation-induced CMA activation downregulated Snail in TNBC cells by promoting cytoplasmic translocation. Evasion of CMA-mediated Snail degradation induced EMT, and enhanced metastatic potential of luminal-type breast cancer cells. Our findings elucidate a previously unrecognized role of CMA in Snail regulation, highlight its significance in breast cancer, and provide a potential therapeutic target for clinical interventions.
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