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Related Experiment Video

Updated: Nov 5, 2025

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

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Chaperonin-Containing TCP1 Complex (CCT) Promotes Breast Cancer Growth Through Correlations With Key Cell Cycle

Heba Ghozlan¹, Adrian Showalter¹, Eunkyung Lee²

¹Division of Cancer Research, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL, United States.

Frontiers in Oncology

|May 17, 2021

Summary

Chaperonin-Containing TCP1 subunit 2 (CCT2) drives breast cancer cell proliferation and anchorage-independent growth. Targeting CCT2 may offer a novel multi-target therapeutic strategy for breast cancer by inhibiting key cell cycle regulators like MYC and cyclin D1.

Keywords:

luminal A node oncogene proliferation targeting tumorigenesis

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Long-term Culture of Human Breast Cancer Specimens and Their Analysis Using Optical Projection Tomography

Long-term Culture of Human Breast Cancer Specimens and Their Analysis Using Optical Projection Tomography

Published on: July 29, 2011

Area of Science:

Oncology
Molecular Biology
Cell Biology

Background:

Dysregulated cell cycling drives cancer proliferation, but drug resistance and limited multi-target inhibitors pose challenges.
Chaperonin-Containing TCP1 (CCT), a protein-folding complex, is implicated in cancer due to its interaction with oncoproteins and tumor suppressors.
CCT subunits, including CCT2, are highly expressed in breast cancer, suggesting a potential role in malignancy.

Purpose of the Study:

To investigate the role of CCT2 in breast cancer cell cycle regulation and proliferation.
To explore CCT2 as a potential therapeutic target for breast cancer treatment.

Main Methods:

Exogenous CCT2-FLAG expression in T47D and MCF7 breast cancer cells.
Assessment of cell proliferation in 2D monolayer and 3D spheroid cultures.
Analysis of gene expression, including MYC, CCND1, and CDK2, and anchorage-independent growth.

Main Results:

CCT2 expression significantly increased breast cancer cell proliferation and spheroid formation.
CCT2-expressing cells exhibited spheroid growth reversal and gained anchorage-independent growth.
CCT2 expression correlated with increased MYC, CCND1, and CDK2 levels, suggesting a role in cell cycle regulation.

Conclusions:

CCT2 acts as a potential oncogene in breast cancer, promoting cell division and growth.
CCT2 may serve as a convergence point for proliferative pathways involving MYC and cyclin D1.
Therapeutic inhibition of CCT2 could offer a multi-target approach to overcome drug resistance in breast cancer.