ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2011
Intracellular clusterin negatively regulates ovarian chemoresistance: compromised expression sensitizes ovarian cancer cells to paclitaxel.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- Glucosylceramide Synthase, a Key Enzyme in Sphingolipid Metabolism, Regulates Expression of Genes Accounting for Cancer Drug Resistance.International journal of molecular sciences · 2025Article
- A comprehensive survey into the role of microRNAs in ovarian cancer chemoresistance; an updated overview.Journal of ovarian research · 2022Review
- MicroRNA-based signatures impacting clinical course and biology of ovarian cancer: a miRNOmics study.Biomarker research · 2021Article
- The multiple roles and therapeutic potential of clusterin in non-small-cell lung cancer: a narrative review.Translational lung cancer research · 2021Review
- NovelFrontiers in chemistry · 2021Article
- The influencing factors and functions of DNA G-quadruplexes.Cell biochemistry and function · 2020Review
- LncRNA DLX6-AS1 aggravates the development of ovarian cancer via modulating FHL2 by sponging miR-195-5p.Cancer cell international · 2020Article
- Heat Shock Proteins and Ovarian Cancer: Important Roles and Therapeutic Opportunities.Cancers · 2019Review
- Inhibition of RNA-Binding Protein Musashi-1 Suppresses Malignant Properties and Reverses Paclitaxel Resistance in Ovarian Carcinoma.Journal of Cancer · 2019Article
- Musashi-1 Expression is a Prognostic Factor in Ovarian Adenocarcinoma and Correlates with ALDH-1 Expression.Pathology oncology research : POR · 2015Article
- Oncogenes associated with drug resistance in ovarian cancer.Journal of cancer research and clinical oncology · 2015Review
- Novel microRNAs expression of patients with chemotherapy drug-resistant and chemotherapy-sensitive epithelial ovarian cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- 7B7: a novel antibody directed against the Ku70/Ku80 heterodimer blocks invasion in pancreatic and lung cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Late-Onset Alzheimer's Disease Genes and the Potentially Implicated Pathways.Current genetic medicine reports · 2014Review
- miR-21 modulates paclitaxel sensitivity and hypoxia-inducible factor-1α expression in human ovarian cancer cells.Oncology letters · 2013Article
- The Role of microRNAs in the Tumorigenesis of Ovarian Cancer.Frontiers in oncology · 2013Article
- Knockdown of clusterin sensitizes pancreatic cancer cells to gemcitabine chemotherapy by ERK1/2 inactivation.Journal of experimental & clinical cancer research : CR · 2012Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Understanding the molecular events that lead to paclitaxel (TX) resistance is necessary to identify effective means to prevent chemoresistance. Previously, results from our lab revealed that secretory clusterin (CLU) form positively mediates TX response in ovarian cancer cells. Thus, we had interest to study the role of another non-secreted form (intracellular clusterin (i-CLU)) in chemo-response. Here, we provide evidences that i-CLU form localizes mainly in the nucleus and differentially expressed in the TX-responsive KF cells, versus TX-resistant, KF-TX, ovarian cancer cells and negatively regulate cellular chemo-response. I-CLU was cloned, by deleting the secretion-leading signaling peptide from full-length CLU cDNA, and transiently over-expressed in OVK-18 cells. Forced expression of truncated i-CLU was mainly detectable in the nuclei and significantly reduced cellular growth, accumulating cells in G1 phase which finally died through apoptosis. Importantly, compromised expression of i-CLU under an inducible promoter was tolerated and did not induce apoptosis but sensitized ovarian cancer cells to TX. We then demonstrated that this sensitization mechanism was cell cycle independent and relied on i-CLU/Ku70 binding probably due to controlling the free amount of Ku70 available for DNA repair in the nucleus. Results from CLU immunohistochemistry in ovarian tumor tissues verified the retardation of nuclear CLU staining in the recurrent tumor even though their primary counterparts showed nuclear CLU staining. Thus, the controversial data on CLU function in chemo-response/resistance may be explained by a shift in the pattern of CLU expression and intracellular localization as well when tumor acquires chemoresistance.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.