Gap Junctions: The Claymore for Cancerous Cells

TL;DR

This study investigates how Carbenoxolone, a gap junction blocker, affects breast cancer cell viability and gene expression, revealing dose-dependent cytotoxic effects and gene regulation changes in cancer cells.

Contribution

It provides new insights into the effects of gap junction blockade on breast cancer cells, highlighting potential mechanisms involving gene regulation and cell viability.

Findings

CBX reduces viability of breast cancer cells dose-dependently

Downregulation of pro- and anti-apoptotic genes observed

CBX affects both low and high proliferative breast cancer cell lines

Abstract

Introduction: Gap junctions play an important role in the cell proliferation in mammalian cells as well as carcinogenesis. However, there are controversial issues about their role in cancer pathogenesis. This study was designed to evaluate genotoxicity and cytotoxicity of Carbenoxolone (CBX) as a prototype of inter-cellular gap junction blocker in MCF7 and BT20 human breast cancer cells. Methods: The MCF7and BT20 human breast cancer cell lines were cultivated, and treated at designated confluency with different doses of CBX. Cellular cytotoxicity was examined using standard colorimetric assay associated with cell viability tests. Gene expression evaluation was carried out using real time polymerase chain reaction (PCR). Results: MCF7 and BT20 cells were significantly affected by CBX in a dose dependent manner in cell viability assays. Despite varying expression of genes, down regulation of pro- and anti-apoptotic genes was observed in these cells. Conclusion: Based upon this investigation, it can be concluded that CBX could affect both low and high proliferative types of breast cancer cell lines and disproportionate down regulation of both pre- and anti-apoptotic genes may be related to interacting biomolecules, perhaps via gap junctions.