Please use this identifier to cite or link to this item: https://doi.org/10.1038/s41388-021-01662-3
Title: Vacuolin-1 inhibits endosomal trafficking and metastasis via CapZ?
Authors: Ye, Zuodong
Wang, Dawei
Lu, Yingying
He, Yunjiao
Yu, Jingting
Wei, Wenjie
Chen, Chang
Wang, Rui
Zhang, Liang
Zhang, Liangren
Le, Minh T. N. 
Cho, William C.
Yang, Mengsu
Zhang, Hongmin
Yue, Jianbo
Issue Date: 9-Feb-2021
Publisher: Springer Nature
Citation: Ye, Zuodong, Wang, Dawei, Lu, Yingying, He, Yunjiao, Yu, Jingting, Wei, Wenjie, Chen, Chang, Wang, Rui, Zhang, Liang, Zhang, Liangren, Le, Minh T. N., Cho, William C., Yang, Mengsu, Zhang, Hongmin, Yue, Jianbo (2021-02-09). Vacuolin-1 inhibits endosomal trafficking and metastasis via CapZ?. Oncogene 40 (10) : 1775-1791. ScholarBank@NUS Repository. https://doi.org/10.1038/s41388-021-01662-3
Rights: Attribution 4.0 International
Abstract: Metastasis is the fundamental cause of cancer mortality, but there are still very few anti-metastatic drugs available. Endosomal trafficking has been implicated in tumor metastasis, and we have previously found that small chemical vacuolin-1 (V1) potently inhibits autophagosome-lysosome fusion and general endosomal-lysosomal degradation. Here, we assessed the anti-metastatic activity of V1 both in vitro and in vivo. V1 significantly inhibits colony formation, migration, and invasion of various cancer cells in vitro. It also compromises the assembly-disassembly dynamics of focal adhesions (FAs) by inhibiting the recycling and degradation of integrins. In various experimental or transgenic mouse models, V1 significantly suppresses the metastasis and/or tumor growth of breast cancer or melanoma. We further identified capping protein Z? (CapZ?) as a V1 binding protein and showed that it is required for the V1-mediated inhibition of migration and metastasis of cancer cells. Collectively, our results indicate that V1 targets CapZ? to inhibit endosomal trafficking and metastasis. © 2021, The Author(s), under exclusive licence to Springer Nature Limited part of Springer Nature.
Source Title: Oncogene
URI: https://scholarbank.nus.edu.sg/handle/10635/232941
ISSN: 0950-9232
DOI: 10.1038/s41388-021-01662-3
Rights: Attribution 4.0 International
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