Cited by 453Clusterin in disease pathologyCell death mechanisms and regulationBiomarkers in Disease Mechanisms

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Clusterin inhibits apoptosis by interacting with activated Bax

Zhang, Honglai, Kim, Jin Koo, Edwards, Chris A., Xu, Zhaohui, Taichman, Russell, Wang, Cun-Yu·2005·Nature Cell Biology

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Abstract

Clusterin is an enigmatic glycoprotein that is overexpressed in several human cancers such as prostate and breast cancers, and squamous cell carcinoma. Because the suppression of clusterin expression renders human cancer cells sensitive to chemotherapeutic drug-mediated apoptosis, it is currently an antisense target in clinical trials for prostate cancer. However, the molecular mechanisms by which clusterin inhibits apoptosis in human cancer cells are unknown. Here we report that intracellular clusterin inhibits apoptosis by interfering with Bax activation in mitochondria. Intriguingly, in contrast to other inhibitors of Bax, clusterin specifically interacts with conformation-altered Bax in response to chemotherapeutic drugs. This interaction impedes Bax oligomerization, which leads to the release of cytochrome c from mitochondria and caspase activation. Moreover, we also find that clusterin inhibits oncogenic c-Myc-mediated apoptosis by interacting with conformation-altered Bax. Clusterin promotes c-Myc-mediated transformation in vitro and tumour progression in vivo. Taken together, our results suggest that the elevated level of clusterin in human cancers may promote oncogenic transformation and tumour progression by interfering with Bax pro-apoptotic activities.

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Authors: Zhang, H., Kim, J. K., Edwards, C. A., Xu, Z., Taichman, R., & Wang, C.-Y.
Affiliations: University of Michigan (US)
Corresponding author: Wang, Cun-Yu
ORCID: Zhang, Honglai
Kim, Jin Koo
Xu, Zhaohui
Taichman, Russell
Venue: Nature Cell Biology
Publisher: Springer Science and Business Media LLC
Published: 2005-08-21
Volume: 7
Issue: 9
Pages: 909-915
ISSN: 1465-7392 (ISSN-L)
1476-4679
DOI: 10.1038/ncb1291
OpenAlex: W2093107372
Cited by: 453
References: 27
Citations by year: 2026: 5 · 2025: 7 · 2024: 13 · 2023: 18 · 2022: 19 · 2021: 22 · 2020: 21 · 2019: 16 · 2018: 19 · 2017: 16 · 2016: 18 · 2015: 20 · 2014: 24 · 2013: 27 · 2012: 31
FWCI: 10.73
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature Cell Biology (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health
Army Research Office
Topics: Health Sciences › Medicine › Oncology › Clusterin in disease pathology
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Life Sciences › Immunology and Microbiology › Immunology › Biomarkers in Disease Mechanisms
Keywords: clusterin, apoptosis inhibition, Bax activation, Bax oligomerization, cytochrome c release, caspase activation, c-Myc, oncogenic transformation, tumor progression, chemosensitization, prostate cancer, breast cancer, squamous cell carcinoma, mitochondrial apoptosis
MeSH terms: Animals, Antineoplastic Agents, Cell Transformation, Neoplastic, Glycoproteins, Humans, Mitochondria, Neoplasms, Protein Conformation, Proto-Oncogene Proteins c-myc, Apoptosis, Molecular Chaperones, Drug Resistance, Neoplasm, Proto-Oncogene Proteins c-bcl-2, Caspases, Cytochromes c, Cell Line, Tumor, bcl-2-Associated X Protein, Clusterin, Rats

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Clusterin inhibits apoptosis by interacting with activated Bax

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