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Related Experiment Video

Updated: Jun 19, 2026

Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms

Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms

Published on: December 9, 2015

Clusterin and chemoresistance.

Julie Y Djeu¹, Sheng Wei

¹Department of Immunology, H. Lee Moffitt Cancer Center, Tampa, Florida 33612, USA.

Advances in Cancer Research

|November 3, 2009

Summary

This summary is machine-generated.

Clusterin (CLU) promotes chemoresistance in various cancers by preventing apoptosis. Targeting the secretory form of clusterin (sCLU) may overcome drug resistance and improve cancer therapy outcomes.

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Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms

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Published on: December 9, 2015

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down

Published on: December 11, 2017

Area of Science:

Oncology
Molecular Biology
Biochemistry

Background:

Anticancer agent resistance is a major obstacle in cancer treatment.
Both intrinsic and acquired resistance mechanisms contribute to therapeutic failure.
Clusterin (CLU) is increasingly recognized as a key factor in chemoresistance.

Purpose of the Study:

To investigate the role of clusterin (CLU) in chemoresistance.
To elucidate the specific form of CLU involved in resistance.
To explore CLU as a potential therapeutic target for overcoming drug resistance.

Main Methods:

Analysis of CLU expression in various cancer types and stages.
Investigating the correlation between CLU expression and resistance to different chemotherapeutic agents.
Examining the antiapoptotic function of secretory CLU (sCLU) by studying its interaction with proteins like Bax and Ku70.

Main Results:

Secretory CLU (sCLU) is upregulated in advanced and metastatic cancers.
sCLU confers broad-based resistance to unrelated chemotherapeutic agents and targeted therapies.
sCLU prevents apoptosis by stabilizing Ku70/Bax complexes, inhibiting cytochrome c release.

Conclusions:

sCLU plays a critical role in preventing apoptosis induced by cytotoxic agents.
sCLU expression is a significant mechanism contributing to chemoresistance in diverse cancers.
Targeting sCLU presents a promising strategy for enhancing the efficacy of cancer therapy.