Ion Channels in Cancer: An Update

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Proliferation and Division".

Deadline for manuscript submissions: 31 July 2025 | Viewed by 1068

Special Issue Editors


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Guest Editor
Department of Integrative Biology and Pharmacology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX 77030, USA
Interests: ion channels; calcium signaling; autophagy; TRP channels; ASICs
Special Issues, Collections and Topics in MDPI journals
1. Department of Integrative Biology and Pharmacology, McGovern Medical School, University of Texas Health Science Center, Houston, TX 77030, USA
2. Biochemistry and Cell Biology Program, Graduate School of Biomedical Sciences, MD Anderson Cancer Center and University of Texas, Houston, TX 77030, USA
Interests: membrane biology; mechanosensing; ras small GTPases; lipidomics; electron microscopy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Membrane voltages have long been observed to contribute to intracellular mitogenic signaling and participate in cell proliferation, survival, and apoptosis. In the brain, the interplay between action potentials and mitogenic signaling is central to long-term potentiation and memory. Pathologically, cancer cells are more depolarized than their normal counterparts. Indeed, targeting ion channels has been suggested as a novel strategy to treat cancer. However, mechanisms underlying the correlation between ion channels and cancer signaling have been largely elusive. This Special Issue focuses on the potential molecular mechanisms mediating how ion channels communicate with intracellular mitogenic cascades and impact cancer signaling.    

Dr. Michael X. Zhu
Dr. Yong Zhou
Guest Editors

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Keywords

  • ion channels
  • cancer therapy
  • cancer cell biology
  • mitogenic signaling
  • cancer signaling

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Research

20 pages, 6017 KiB  
Article
Expression Profiling Identified TRPM7 and HER2 as Potential Targets for the Combined Treatment of Cancer Cells
by Miyuki Egawa, Eva Schmücker, Christian Grimm, Thomas Gudermann and Vladimir Chubanov
Cells 2024, 13(21), 1801; https://doi.org/10.3390/cells13211801 - 31 Oct 2024
Viewed by 837
Abstract
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 [...] Read more.
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 TRPM7 gene introduced by the CRISPR/Cas9 approach. This analysis revealed that TRPM7 regulates the expression levels of several transcripts, including HER2 (ERBB2). Consequently, we examined the TRPM7/HER2 axis in several non-hematopoietic cells to show that TRPM7 affects the expression of HER2 protein in a Zn2+-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. Full article
(This article belongs to the Special Issue Ion Channels in Cancer: An Update)
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