TRPV2 calcium channel promotes breast cancer progression potential by activating autophagy
Breast cancer, the most prevalent and aggressive tumor affecting women, requires identification of disease determinants to facilitate the development of effective therapeutic strategies. Transient receptor potential vanilloid 2 (TRPV2), an ion channel highly permeable for calcium (Ca<sup>2+</sup>), is implicated in physiological and pathological processes. Nevertheless, the role of TRPV2 in breast cancer remains poorly elucidated. In this study, we found high levels of TRPV2 expression associated with advanced malignancy, thereby suggesting its potential as a biomarker for breast cancer staging. We demonstrated that TRPV2 activation promotes breast cancer cell proliferation, migration, and invasion, while silencing of TRPV2 suppresses breast cancer progression, highlighting the oncogenic role of TRPV2. Moreover, we reveal that TRPV2 facilitates cancer progression by modulating the CaMKKβ/AMPK/ULK1-autophagic axis through mediating calcium influx, providing new insights into TRPV2 as a novel therapeutic target for breast cancer treatment.
Authors
- Lai K. Leung (ORCID: https://orcid.org/0000-0002-7781-3099)
- Xiaoqiang Yao (ORCID: https://orcid.org/0000-0002-0687-8186)
- William Chi Shing Cho (ORCID: https://orcid.org/0000-0003-4174-4586)
- Gary Man-Kit Tse (ORCID: https://orcid.org/0000-0002-9405-9665)
- Qing Li (ORCID: https://orcid.org/0000-0001-7933-1619)
- Huixian Li (ORCID: https://orcid.org/0000-0001-5722-8602)
- Wing Tak Wong
- Fung Ping Leung
- Ruiwen Zhu
Institutions
- Chinese University of Hong Kong (HK)
- Queen Elizabeth Hospital (GB)
- Hong Kong Biotechnology Organization (CN)
- Second Hospital of Tianjin Medical University (CN)
- Metropolitan University (BD)
- Tianjin Medical University (CN)
- University of Hong Kong (HK)
Publication Details
- Journal
- Cancer Cell International
- Published
- 2024-09-27
- DOI
- https://doi.org/10.1186/s12935-024-03506-y
- Citations
- 6
- Primary Topic
- Ion Channels and Receptors
- Type
- article
- Field-Weighted Citation Impact
- 2.17
Funders
- National Natural Science Foundation of China