Expression Profiling Identified TRPM7 and HER2 as Potential Targets for the Combined Treatment of Cancer Cells

TRPM7 is a divalent cation-permeable channel that is highly active in cancer cells. The pharmacological inhibitors of TRPM7 have been shown to suppress the proliferation of tumor cells, highlighting TRPM7 as a new anticancer drug target. However, the potential benefit of combining TRPM7 inhibitors w...

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Main Authors: Miyuki Egawa, Eva Schmücker, Christian Grimm, Thomas Gudermann, Vladimir Chubanov
Format: Article
Language:English
Published: MDPI AG 2024-10-01
Series:Cells
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Online Access:https://www.mdpi.com/2073-4409/13/21/1801
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author Miyuki Egawa
Eva Schmücker
Christian Grimm
Thomas Gudermann
Vladimir Chubanov
author_facet Miyuki Egawa
Eva Schmücker
Christian Grimm
Thomas Gudermann
Vladimir Chubanov
author_sort Miyuki Egawa
collection DOAJ
description TRPM7 is a divalent cation-permeable channel that is highly active in cancer cells. The pharmacological inhibitors of TRPM7 have been shown to suppress the proliferation of tumor cells, highlighting TRPM7 as a new anticancer drug target. However, the potential benefit of combining TRPM7 inhibitors with conventional anticancer therapies remains unexplored. Here, we used genome-wide transcriptome profiling of human leukemia HAP1 cells to examine cellular responses caused by the application of NS8593, the potent inhibitor of the TRPM7 channel, in comparison with two independent knockout mutations in the <i>TRPM7</i> gene introduced by the CRISPR/Cas9 approach. This analysis revealed that <i>TRPM7</i> regulates the expression levels of several transcripts, including <i>HER2</i> (<i>ERBB2</i>). Consequently, we examined the <i>TRPM7/HER2</i> axis in several non-hematopoietic cells to show that TRPM7 affects the expression of HER2 protein in a Zn<sup>2+</sup>-dependent fashion. Moreover, we found that co-administration of pharmacological inhibitors of HER2 and TRPM7 elicited a synergistic antiproliferative effect on HER2-overexpressing SKBR3 cells but not on HER2-deficient MDA-MB-231 breast cancer cells. Hence, our study proposes a new combinatorial strategy for treating HER2-positive breast cancer cells.
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spelling doaj-art-d11788bdb0914527a0cc4af05542b0f62024-11-08T14:34:33ZengMDPI AGCells2073-44092024-10-011321180110.3390/cells13211801Expression Profiling Identified TRPM7 and HER2 as Potential Targets for the Combined Treatment of Cancer CellsMiyuki Egawa0Eva Schmücker1Christian Grimm2Thomas Gudermann3Vladimir Chubanov4Walther-Straub Institute of Pharmacology and Toxicology, Ludwig Maximilian University of Munich, 80336 Munich, GermanyWalther-Straub Institute of Pharmacology and Toxicology, Ludwig Maximilian University of Munich, 80336 Munich, GermanyWalther-Straub Institute of Pharmacology and Toxicology, Ludwig Maximilian University of Munich, 80336 Munich, GermanyWalther-Straub Institute of Pharmacology and Toxicology, Ludwig Maximilian University of Munich, 80336 Munich, GermanyWalther-Straub Institute of Pharmacology and Toxicology, Ludwig Maximilian University of Munich, 80336 Munich, GermanyTRPM7 is a divalent cation-permeable channel that is highly active in cancer cells. The pharmacological inhibitors of TRPM7 have been shown to suppress the proliferation of tumor cells, highlighting TRPM7 as a new anticancer drug target. However, the potential benefit of combining TRPM7 inhibitors with conventional anticancer therapies remains unexplored. Here, we used genome-wide transcriptome profiling of human leukemia HAP1 cells to examine cellular responses caused by the application of NS8593, the potent inhibitor of the TRPM7 channel, in comparison with two independent knockout mutations in the <i>TRPM7</i> gene introduced by the CRISPR/Cas9 approach. This analysis revealed that <i>TRPM7</i> regulates the expression levels of several transcripts, including <i>HER2</i> (<i>ERBB2</i>). Consequently, we examined the <i>TRPM7/HER2</i> axis in several non-hematopoietic cells to show that TRPM7 affects the expression of HER2 protein in a Zn<sup>2+</sup>-dependent fashion. Moreover, we found that co-administration of pharmacological inhibitors of HER2 and TRPM7 elicited a synergistic antiproliferative effect on HER2-overexpressing SKBR3 cells but not on HER2-deficient MDA-MB-231 breast cancer cells. Hence, our study proposes a new combinatorial strategy for treating HER2-positive breast cancer cells.https://www.mdpi.com/2073-4409/13/21/1801TRP channelsHER2ERBB2NS8593CP724714zinc
spellingShingle Miyuki Egawa
Eva Schmücker
Christian Grimm
Thomas Gudermann
Vladimir Chubanov
Expression Profiling Identified TRPM7 and HER2 as Potential Targets for the Combined Treatment of Cancer Cells
Cells
TRP channels
HER2
ERBB2
NS8593
CP724714
zinc
title Expression Profiling Identified TRPM7 and HER2 as Potential Targets for the Combined Treatment of Cancer Cells
title_full Expression Profiling Identified TRPM7 and HER2 as Potential Targets for the Combined Treatment of Cancer Cells
title_fullStr Expression Profiling Identified TRPM7 and HER2 as Potential Targets for the Combined Treatment of Cancer Cells
title_full_unstemmed Expression Profiling Identified TRPM7 and HER2 as Potential Targets for the Combined Treatment of Cancer Cells
title_short Expression Profiling Identified TRPM7 and HER2 as Potential Targets for the Combined Treatment of Cancer Cells
title_sort expression profiling identified trpm7 and her2 as potential targets for the combined treatment of cancer cells
topic TRP channels
HER2
ERBB2
NS8593
CP724714
zinc
url https://www.mdpi.com/2073-4409/13/21/1801
work_keys_str_mv AT miyukiegawa expressionprofilingidentifiedtrpm7andher2aspotentialtargetsforthecombinedtreatmentofcancercells
AT evaschmucker expressionprofilingidentifiedtrpm7andher2aspotentialtargetsforthecombinedtreatmentofcancercells
AT christiangrimm expressionprofilingidentifiedtrpm7andher2aspotentialtargetsforthecombinedtreatmentofcancercells
AT thomasgudermann expressionprofilingidentifiedtrpm7andher2aspotentialtargetsforthecombinedtreatmentofcancercells
AT vladimirchubanov expressionprofilingidentifiedtrpm7andher2aspotentialtargetsforthecombinedtreatmentofcancercells