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Cells
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Ion Channels in Cancer
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Ion Channels in Cancer

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Biophysics".

Deadline for manuscript submissions: closed (15 August 2023) | Viewed by 5031

Special Issue Editors

Dr. Michael X. Zhu

E-Mail Website
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
Dr. Yong Zhou

E-Mail Website
Guest Editor
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 potential 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 ellusive. The current 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

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Related Special Issue

Published Papers (3 papers)

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Research

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22 pages, 2888 KiB  
Article
Contribution of the α5 nAChR Subunit and α5SNP to Nicotine-Induced Proliferation and Migration of Human Cancer Cells
by Irida Papapostolou, Daniela Ross-Kaschitza, Florian Bochen, Christine Peinelt and Maria Constanza Maldifassi
Cells 2023, 12(15), 2000; https://doi.org/10.3390/cells12152000 - 04 Aug 2023
Cited by 2 | Viewed by 1308
Abstract
Nicotine in tobacco is known to induce tumor-promoting effects and cause chemotherapy resistance through the activation of nicotinic acetylcholine receptors (nAChRs). Many studies have associated the α5 nicotinic receptor subunit (α5), and a specific polymorphism in this subunit, with (i) nicotine administration, (ii) [...] Read more.
Nicotine in tobacco is known to induce tumor-promoting effects and cause chemotherapy resistance through the activation of nicotinic acetylcholine receptors (nAChRs). Many studies have associated the α5 nicotinic receptor subunit (α5), and a specific polymorphism in this subunit, with (i) nicotine administration, (ii) nicotine dependence, and (iii) lung cancer. The α5 gene CHRNA5 mRNA is upregulated in several types of cancer, including lung, prostate, colorectal, and stomach cancer, and cancer severity is correlated with smoking. In this study, we investigate the contribution of α5 in the nicotine-induced cancer hallmark functions proliferation and migration, in breast, colon, and prostate cancer cells. Nine human cell lines from different origins were used to determine nAChR subunit expression levels. Then, selected breast (MCF7), colon (SW480), and prostate (DU145) cancer cell lines were used to investigate the nicotine-induced effects mediated by α5. Using pharmacological and siRNA-based experiments, we show that α5 is essential for nicotine-induced proliferation and migration. Additionally, upon downregulation of α5, nicotine-promoted expression of EMT markers and immune regulatory proteins was impaired. Moreover, the α5 polymorphism D398N (α5SNP) caused a basal increase in proliferation and migration in the DU145 cell line, and the effect was mediated through G-protein signaling. Taken together, our results indicate that nicotine-induced cancer cell proliferation and migration are mediated via α5, adding to the characterization of α5 as a putative therapeutical target. Full article
(This article belongs to the Special Issue Ion Channels in Cancer)
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24 pages, 9912 KiB  
Article
Modulation of Lysosomal Cl− Mediates Migration and Apoptosis through the TRPML1 as a Lysosomal Cl− Sensor
by Dongun Lee and Jeong Hee Hong
Cells 2023, 12(14), 1835; https://doi.org/10.3390/cells12141835 - 12 Jul 2023
Cited by 1 | Viewed by 1019
Abstract
Lysosomes are responsible for protein degradation and clearance in cellular recycling centers. It has been known that the lysosomal chloride level is enriched and involved in the intrinsic lysosomal function. However, the mechanism by which chloride levels can be sensed and that of [...] Read more.
Lysosomes are responsible for protein degradation and clearance in cellular recycling centers. It has been known that the lysosomal chloride level is enriched and involved in the intrinsic lysosomal function. However, the mechanism by which chloride levels can be sensed and that of the chloride-mediated lysosomal function is unknown. In this study, we verified that reduced chloride levels acutely induced lysosomal calcium release through TRPML1 and lysosomal repositioning toward the juxtanuclear region. Functionally, low chloride-induced lysosomal calcium release attenuated cellular migration. In addition, spontaneous exposure to low chloride levels dysregulated lysosomal biogenesis and subsequently induced delayed migration and promoted apoptosis. Two chloride-sensing GXXXP motifs in the TRPML1 were identified. Mutations in the GXXXP motif of TRPML1 did not affect chloride levels, and there were no changes in migratory ability. In this study, we demonstrated that the depletion of chloride induces reformation of the lysosomal calcium pool and subsequently dysregulated cancer progression, which will assist in improving therapeutic strategies for lysosomal accumulation-associated diseases or cancer cell apoptosis. Full article
(This article belongs to the Special Issue Ion Channels in Cancer)
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Review

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26 pages, 1117 KiB  
Review
To Be or Not to Be an Ion Channel: Cryo-EM Structures Have a Say
by Gui-Lan Chen, Jian Li, Jin Zhang and Bo Zeng
Cells 2023, 12(14), 1870; https://doi.org/10.3390/cells12141870 - 17 Jul 2023
Cited by 2 | Viewed by 2331
Abstract
Ion channels are the second largest class of drug targets after G protein-coupled receptors. In addition to well-recognized ones like voltage-gated Na/K/Ca channels in the heart and neurons, novel ion channels are continuously discovered in both excitable and non-excitable cells and demonstrated to [...] Read more.
Ion channels are the second largest class of drug targets after G protein-coupled receptors. In addition to well-recognized ones like voltage-gated Na/K/Ca channels in the heart and neurons, novel ion channels are continuously discovered in both excitable and non-excitable cells and demonstrated to play important roles in many physiological processes and diseases such as developmental disorders, neurodegenerative diseases, and cancer. However, in the field of ion channel discovery, there are an unignorable number of published studies that are unsolid and misleading. Despite being the gold standard of a functional assay for ion channels, electrophysiological recordings are often accompanied by electrical noise, leak conductance, and background currents of the membrane system. These unwanted signals, if not treated properly, lead to the mischaracterization of proteins with seemingly unusual ion-conducting properties. In the recent ten years, the technical revolution of cryo-electron microscopy (cryo-EM) has greatly advanced our understanding of the structures and gating mechanisms of various ion channels and also raised concerns about the pore-forming ability of some previously identified channel proteins. In this review, we summarize cryo-EM findings on ion channels with molecular identities recognized or disputed in recent ten years and discuss current knowledge of proposed channel proteins awaiting cryo-EM analyses. We also present a classification of ion channels according to their architectures and evolutionary relationships and discuss the possibility and strategy of identifying more ion channels by analyzing structures of transmembrane proteins of unknown function. We propose that cross-validation by electrophysiological and structural analyses should be essentially required for determining molecular identities of novel ion channels. Full article
(This article belongs to the Special Issue Ion Channels in Cancer)
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