Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.4
5.2
Journals
Cancers
Special Issues
The Emerging Role of Ion Channels in Cancer Treatment
share announcement

The Emerging Role of Ion Channels in Cancer Treatment

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Therapy".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 1239

Special Issue Editor

Dr. V'yacheslav Lehen'kyi

E-Mail Website
Guest Editor
Laboratory of Cell Physiology, INSERM U1003, Laboratory of Excellence Ion Channels Science and Therapeutics, Department of Biology, Faculty of Science and Technologies, University of Lille, 59650 Villeneuve d'Ascq, France
Interests: ion channels; calcium; TRPV6; tumor targeting in vivo; innovative therapy

Special Issue Information

Dear Colleagues,

A considerable amount of evidence has been demonstrated to date regarding the role of ion channels in all essential processes of carcinogenesis, including cell proliferation, apoptosis resistance, migration, invasion, angiogenesis, etc. In fact, ion signaling is strongly involved in the vast majority, if not in all, of the cell regulation processes, both normal and pathophysiological. Thus, targeting ion channels represents a prospective treatment, particularly when used in combination with the existing cell-toxic drugs. Recently, it has been demonstrated that ion channels may be involved in anti-cancer drug resistance, and thus their targeting would provide a benefit for patients, especially in the framework of precision therapy.

The focus of this Special Issue is thus to consider ion channel regulation as well as downstream signaling in cancer treatment and drug resistance.

Dr. V'yacheslav Lehen'kyi
Guest Editor

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. Cancers 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 2900 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.

Keywords

  • ion channels
  • ion signaling
  • tumor targeting
  • cancer treatment
  • therapy resistance
  • precision therapy

Published Papers (1 paper)

Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

22 pages, 9514 KiB  
Article
TRPV6 Channel Is Involved in Pancreatic Ductal Adenocarcinoma Aggressiveness and Resistance to Chemotherapeutics
by Gonçalo Mesquita, Aurélien Haustrate, Adriana Mihalache, Benjamin Soret, Clément Cordier, Emilie Desruelles, Erika Duval, Zoltan Pethö, Natalia Prevarskaya, Albrecht Schwab and V’yacheslav Lehen’kyi
Cancers 2023, 15(24), 5769; https://doi.org/10.3390/cancers15245769 - 08 Dec 2023
Viewed by 893
Abstract
Pancreatic ductal adenocarcinoma (PDAC) stands as a highly aggressive and lethal cancer, characterized by a grim prognosis and scarce treatment alternatives. Within this context, TRPV6, a calcium-permeable channel, emerges as a noteworthy candidate due to its overexpression in various cancers, capable of influencing [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) stands as a highly aggressive and lethal cancer, characterized by a grim prognosis and scarce treatment alternatives. Within this context, TRPV6, a calcium-permeable channel, emerges as a noteworthy candidate due to its overexpression in various cancers, capable of influencing the cell behavior in different cancer entities. Nonetheless, the exact expression pattern and functional significance of TRPV6 in the context of PDAC remains enigmatic. This study scrutinizes the expression of TRPV6 in tissue specimens obtained from 46 PDAC patients across distinct stages and grades. We manipulated TRPV6 expression (knockdown, overexpression) in the human PDAC cell lines Panc-1 and Capan-1. Subsequently, we analyzed its impact on multiple facets, encompassing Ca2+ influx, proliferation, apoptosis, migration, chemoresistance, and tumor growth, both in vitro and in vivo. Notably, the data indicate a direct correlation between TRPV6 expression levels, tumor stage, and grade, establishing a link between TRPV6 and PDAC proliferation in tissue samples. Decreasing TRPV6 expression via knockdown hampered Ca2+ influx, resulting in diminished proliferation and viability in both cell lines, and cell cycle progression in Panc-1. The knockdown simultaneously led to an increase in apoptotic rates and increased the susceptibility of cells to 5-FU and gemcitabine treatments. Moreover, it accelerated migration and promoted collective movement among Panc-1 cells. Conversely, TRPV6 overexpression yielded opposing outcomes in terms of proliferation in Panc-1 and Capan-1, and the migration of Panc-1 cells. Intriguingly, both TRPV6 knockdown and overexpression diminished the process of tumor formation in vivo. This intricate interplay suggests that PDAC aggressiveness relies on a fine-tuned TRPV6 expression, raising its profile as a putative therapeutic target. Full article
(This article belongs to the Special Issue The Emerging Role of Ion Channels in Cancer Treatment)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-1
Back to TopTop