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Related Experiment Video

Updated: Jun 19, 2026

In vivo and in vitro Studies of Adaptor-clathrin Interaction

In vivo and in vitro Studies of Adaptor-clathrin Interaction

Published on: January 26, 2011

CLU "in and out": looking for a link.

Sabina Pucci¹, P Mazzarelli, C Nucci

¹Department of Biopathology, Institute of Anatomic Pathology, University of Rome Tor Vergata, 00133 Rome, Italy.

Advances in Cancer Research

|November 3, 2009

Summary

Tumor progression relies on cancer cell interactions with the microenvironment. Clusterin (CLU) has dual roles, acting as a prosurvival factor or tumor suppressor, influenced by its microenvironment.

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Area of Science:

Oncology
Molecular Biology
Cancer Microenvironment Research

Background:

Tumor progression and metastasis are critically dependent on synergistic interactions between cancer cells and their surrounding microenvironment.
The tumor microenvironment influences cancer cell behavior through epigenetic modifications and the exchange of soluble factors.
Clusterin (CLU) is an enigmatic protein with diverse, often opposing, functions, acting both intracellularly and extracellularly.

Purpose of the Study:

To review the intricate relationship between tumor microenvironment interactions and the regulation of Clusterin (CLU) expression and function.
To explore the pleiotropic actions of extracellular CLU (sCLU) in modulating stromal dynamics and intercellular communication.
To highlight the potential of CLU as a therapeutic target in cancer treatment strategies.

Main Methods:

Literature review focusing on tumor-microenvironment interactions and Clusterin (CLU) biology.
Analysis of existing data on the dual roles of CLU in cancer cell survival, genome stability, and tumor suppression.
Examination of the impact of extracellular CLU (sCLU) on stromal cells and chemokine secretion.

Main Results:

The tumor microenvironment significantly dictates the expression and function of different CLU forms, influencing cancer growth, invasion, and metastasis.
Extracellular CLU (sCLU) actively reprograms stromal components, alters cell-cell signaling, and impacts chemokine profiles.
CLU exhibits context-dependent functions, acting as a prosurvival chaperone or a tumor suppressor by interacting with DNA repair proteins and cell death inducers.

Conclusions:

Understanding the 'in and out' functions of CLU within the tumor microenvironment is crucial for deciphering cancer progression.
The complex interplay between CLU, cytokines, and stromal cells offers potential therapeutic avenues.
Further research into CLU's multifaceted roles may lead to novel co-targeting strategies for cancer therapy.