The vital role of TRPM2 in breast cancer cell proliferation and its difference in expression between non-Hispanic white and non-Hispanic black females
WCRJ 2025;
12
: e2870
DOI: 10.32113/wcrj_20255_2870
Topic: Breast cancer
Category: Original article
Abstract
Objective: To study the racial disparity of transient receptor potential melastatin-related channel subtype 2 (TRPM2) expression in non-Hispanic black (NHB) women and non-Hispanic white women (NHW) breast cancer tissues. Specific roles of TRPM2 in the proliferation and apoptosis of the human mitogenic breast cancer cells (MCF-7 ER+) are also investigated.
Materials and Methods: TRPM2 expression analysis was performed using the normalized mRNA expression data downloaded from Broad GDAC Firehose. The functions of TRPM2 in normal and cancer cells are revealed using patch-clamp recording and intracellular calcium imaging techniques.
Results: TRPM2 is expressed at different levels in breast ductal and lobular neoplasm disease between NHB and NHW. Selective knock-down of TRPM2 mRNA with small interfering RNA (siRNA/TRPM2) caused substantial inhibition of cell proliferation of MCF-7(ER+) cells but not in the control human mammary epithelial (HME) cells. The siRNA/TRPM2 also induced cellular apoptosis in MCF-7(ER+) cells but not HME cells. Immunofluorescent staining shows that TRPM2 abnormally localizes in the MCF-7(ER+) nuclei but not HME cells.
Conclusions: These results suggest that TRPM2 is essential in promoting MCF-7(ER+) cell proliferation and may be a potential target for breast cancer treatment.
Materials and Methods: TRPM2 expression analysis was performed using the normalized mRNA expression data downloaded from Broad GDAC Firehose. The functions of TRPM2 in normal and cancer cells are revealed using patch-clamp recording and intracellular calcium imaging techniques.
Results: TRPM2 is expressed at different levels in breast ductal and lobular neoplasm disease between NHB and NHW. Selective knock-down of TRPM2 mRNA with small interfering RNA (siRNA/TRPM2) caused substantial inhibition of cell proliferation of MCF-7(ER+) cells but not in the control human mammary epithelial (HME) cells. The siRNA/TRPM2 also induced cellular apoptosis in MCF-7(ER+) cells but not HME cells. Immunofluorescent staining shows that TRPM2 abnormally localizes in the MCF-7(ER+) nuclei but not HME cells.
Conclusions: These results suggest that TRPM2 is essential in promoting MCF-7(ER+) cell proliferation and may be a potential target for breast cancer treatment.
To cite this article
The vital role of TRPM2 in breast cancer cell proliferation and its difference in expression between non-Hispanic white and non-Hispanic black females
WCRJ 2025;
12
: e2870
DOI: 10.32113/wcrj_20255_2870
Publication History
Submission date: 29 Jul 2024
Revised on: 02 Sep 2024
Accepted on: 23 Dec 2024
Published online: 07 May 2025

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