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Myo1b promotes tumor progression and angiogenesis by inhibiting autophagic degradation of HIF-1α in colorectal cancer

Myosin 1b (Myo1b) is an important single-headed membrane-associated motor of class I myosins that participate in many critical physiological and pathological processes. Mounting evidence suggests that the dysregulation of Myo1b expression has been extensively investigated in the development and prog...

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Autores principales: Chen, Yi-Hong, Xu, Nan-Zhu, Hong, Chang, Li, Wen-Qi, Zhang, Yi-Qiong, Yu, Xin-Yi, Huang, Yue-Le, Zhou, Jue-Yu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9643372/
https://www.ncbi.nlm.nih.gov/pubmed/36347835
http://dx.doi.org/10.1038/s41419-022-05397-1
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author Chen, Yi-Hong
Xu, Nan-Zhu
Hong, Chang
Li, Wen-Qi
Zhang, Yi-Qiong
Yu, Xin-Yi
Huang, Yue-Le
Zhou, Jue-Yu
author_facet Chen, Yi-Hong
Xu, Nan-Zhu
Hong, Chang
Li, Wen-Qi
Zhang, Yi-Qiong
Yu, Xin-Yi
Huang, Yue-Le
Zhou, Jue-Yu
author_sort Chen, Yi-Hong
collection PubMed
description Myosin 1b (Myo1b) is an important single-headed membrane-associated motor of class I myosins that participate in many critical physiological and pathological processes. Mounting evidence suggests that the dysregulation of Myo1b expression has been extensively investigated in the development and progression of several tumors. However, the functional mechanism of Myo1b in CRC angiogenesis and autophagy progression remains unclear. Herein, we found that the expression of Myo1b was upregulated in CRC tissues and its high expression was correlated with worse survival. The overexpression of Myo1b promoted the proliferation, migration and invasion of CRC cells. Conversely, silencing of Myo1b suppressed tumor progression both in vitro and in vivo. Further studies indicated that Myo1b inhibited the autophagosome-lysosome fusion and potentiated the VEGF secretion of CRC cells to promote angiogenesis. Mechanistically, Myo1b blocked the autophagic degradation of HIF-1α and then led to the accumulation of HIF-1α, thus enhancing VEGF secretion and then promoting tumor angiogenesis in CRC. Together, our study provided novel insights into the role of Myo1b in CRC progression and revealed that it might be a feasible predictive biomarker and promising therapeutic target for CRC patients.
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spelling pubmed-96433722022-11-15 Myo1b promotes tumor progression and angiogenesis by inhibiting autophagic degradation of HIF-1α in colorectal cancer Chen, Yi-Hong Xu, Nan-Zhu Hong, Chang Li, Wen-Qi Zhang, Yi-Qiong Yu, Xin-Yi Huang, Yue-Le Zhou, Jue-Yu Cell Death Dis Article Myosin 1b (Myo1b) is an important single-headed membrane-associated motor of class I myosins that participate in many critical physiological and pathological processes. Mounting evidence suggests that the dysregulation of Myo1b expression has been extensively investigated in the development and progression of several tumors. However, the functional mechanism of Myo1b in CRC angiogenesis and autophagy progression remains unclear. Herein, we found that the expression of Myo1b was upregulated in CRC tissues and its high expression was correlated with worse survival. The overexpression of Myo1b promoted the proliferation, migration and invasion of CRC cells. Conversely, silencing of Myo1b suppressed tumor progression both in vitro and in vivo. Further studies indicated that Myo1b inhibited the autophagosome-lysosome fusion and potentiated the VEGF secretion of CRC cells to promote angiogenesis. Mechanistically, Myo1b blocked the autophagic degradation of HIF-1α and then led to the accumulation of HIF-1α, thus enhancing VEGF secretion and then promoting tumor angiogenesis in CRC. Together, our study provided novel insights into the role of Myo1b in CRC progression and revealed that it might be a feasible predictive biomarker and promising therapeutic target for CRC patients. Nature Publishing Group UK 2022-11-08 /pmc/articles/PMC9643372/ /pubmed/36347835 http://dx.doi.org/10.1038/s41419-022-05397-1 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Chen, Yi-Hong
Xu, Nan-Zhu
Hong, Chang
Li, Wen-Qi
Zhang, Yi-Qiong
Yu, Xin-Yi
Huang, Yue-Le
Zhou, Jue-Yu
Myo1b promotes tumor progression and angiogenesis by inhibiting autophagic degradation of HIF-1α in colorectal cancer
title Myo1b promotes tumor progression and angiogenesis by inhibiting autophagic degradation of HIF-1α in colorectal cancer
title_full Myo1b promotes tumor progression and angiogenesis by inhibiting autophagic degradation of HIF-1α in colorectal cancer
title_fullStr Myo1b promotes tumor progression and angiogenesis by inhibiting autophagic degradation of HIF-1α in colorectal cancer
title_full_unstemmed Myo1b promotes tumor progression and angiogenesis by inhibiting autophagic degradation of HIF-1α in colorectal cancer
title_short Myo1b promotes tumor progression and angiogenesis by inhibiting autophagic degradation of HIF-1α in colorectal cancer
title_sort myo1b promotes tumor progression and angiogenesis by inhibiting autophagic degradation of hif-1α in colorectal cancer
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9643372/
https://www.ncbi.nlm.nih.gov/pubmed/36347835
http://dx.doi.org/10.1038/s41419-022-05397-1
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