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Published on: June 9, 2023
Evidence that TRPM7 is required for breast cancer cell proliferation
Arnaud Guilbert1, Mathieu Gautier, Isabelle Dhennin-Duthille
1Laboratoire de Physiologie Cellulaire et Moléculaire, Univ. Picardie Jules Verne, Faculté des Sciences, 33 Rue St Leu, 80000 Amiens, France.
Abstract:
Because transient receptor potential (TRP) channels have been implicated in tumor progression, we have investigated the potential role of TRPM7 channel in breast cancer cell proliferation. Under whole cell patch clamp, a Mg(2+)-inhibited cationic (MIC) current was observed in MCF-7 cells. This current was characterized by an inward current and a strong outward rectifying current that were both inhibited in a concentration-dependent manner by the presence of intracellular Mg(2+) or Mg(2+)-ATP. The inward current was reduced by La(3+), and the outward current was sensitive to 2-aminoethoxydiphenyl borate (2-APB), spermine, La(3+), and flufenamic acid. Importantly, a similar MIC current was also recorded in the primary culture of human breast cancerous epithelial cells (hBCE). Moreover, TRPM7 transcripts were found in both hBCE and MCF-7 cells. In MCF-7 cells, the MIC current was inhibited by TRPM7 small interfering RNA. Interestingly, we found that cell proliferation and intracellular Ca(2+) concentration were also reduced by TRPM7 silencing in MCF-7 cells. TRPM7 channels were also found in both human breast cancer and healthy tissues. Importantly, TRPM7 channel was overexpressed in grade III breast cancer samples associated with important Ki67 or tumor size. Our findings strongly suggest that TRPM7 is involved in the proliferative potentiality of breast cancer cells, probably by regulating Ca(2+) influx.
Insights
The transient receptor potential melastatin 7 (TRPM7) channel promotes breast cancer cell proliferation. Silencing TRPM7 reduced cancer cell growth and calcium levels, suggesting it
Area of Science:
- Molecular Biology
- Oncology
- Ion Channel Physiology
Background:
- Transient receptor potential (TRP) channels are implicated in cancer progression.
- The specific role of TRPM7 in breast cancer proliferation requires further investigation.
Purpose of the Study:
- To investigate the role of the TRPM7 channel in breast cancer cell proliferation.
- To characterize the Mg(2+)-inhibited cationic (MIC) current in breast cancer cells.
Main Methods:
- Whole-cell patch clamp electrophysiology to record MIC currents in MCF-7 and human breast cancerous epithelial (hBCE) cells.
- TRPM7 gene expression analysis using transcript detection.
- TRPM7 small interfering RNA (siRNA) to silence gene expression.
- Cell proliferation assays and intracellular calcium concentration measurements.
Main Results:
- A Mg(2+)-inhibited cationic (MIC) current, sensitive to various modulators, was identified in MCF-7 and hBCE cells.
- TRPM7 transcripts were detected in both cell types, and TRPM7 siRNA inhibited the MIC current in MCF-7 cells.
- TRPM7 silencing reduced MCF-7 cell proliferation and intracellular calcium concentration.
- TRPM7 was overexpressed in grade III breast cancer tissues, correlating with Ki67 and tumor size.
Conclusions:
- TRPM7 channels are present and functional in breast cancer cells.
- TRPM7 plays a significant role in breast cancer cell proliferation, likely through regulating calcium influx.
- TRPM7 overexpression in advanced breast cancer suggests its potential as a therapeutic target.
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