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Special Issue Editor

Special Issue Information

Dear Colleagues,

Calcium signaling plays a critical role in orchestrating diverse cellular processes, ranging from muscle contraction to neuronal plasticity and from cell growth to cell death. Intracellular Ca²⁺ signals are mediated by components of the calcium signaling toolkit, including calcium channels, pumps, exchangers, and regulators. Ca²⁺ signaling, in addition to its various physiological roles, is also involved in pathological conditions including cancer. Indeed, calcium signaling controls several “cancer hallmarks”. Dysregulation in the expression and/or activity of Ca²⁺-regulating proteins is implicated in different types of cancers, where it promotes specific oncogenic processes. Understanding the role and regulation of calcium signaling in cancer provides critical information about cancer biology and may pave the way for the development of novel therapeutic approaches.

We are pleased to invite you to contribute to this Special Issue on “regulation, role and targeting of calcium signaling pathways in cancer”. This Special Issue aims to present novel insights into the diverse roles of Ca²⁺ signaling pathways and regulators in cancer initiation and progression. It also focuses on the potential therapeutic and diagnostic opportunities this may provide.

In this Special Issue, original research articles and reviews are welcome. Topics may include (but are not limited to) the following:

The activity and regulation of calcium signaling pathways in cancer cells;
The role of calcium signaling and calcium signaling toolkits in cancer initiation and/or the progression of cancer-associated processes;
The altered expression of calcium-regulating genes/protein in cancer;
The genetic/pharmacological targeting of calcium signaling pathways as a potential novel therapeutic approach in cancer.

We look forward to receiving your contributions.

Dr. Iman Azimi
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

calcium signaling
cancer
targeted therapy
biomarkers
diagnosis
calcium channels and pumps
cytosolic Ca²⁺
organellar Ca²⁺

Published Papers (2 papers)

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Research

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27 pages, 5692 KiB

Open AccessArticle

Acid Adaptation Promotes TRPC1 Plasma Membrane Localization Leading to Pancreatic Ductal Adenocarcinoma Cell Proliferation and Migration through Ca²⁺ Entry and Interaction with PI3K/CaM

by Julie Schnipper, Sana Kouba, Frédéric Hague, Alban Girault, Marie-Sophie Telliez, Stéphanie Guénin, Ahmed Ahidouch, Stine Falsig Pedersen and Halima Ouadid-Ahidouch

Cancers 2022, 14(19), 4946; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14194946 - 09 Oct 2022

Cited by 2 | Viewed by 1574

Abstract

Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal malignancies, with a low overall survival rate of less than 10% and limited therapeutic options. Fluctuations in tumor microenvironment pH are a hallmark of PDAC development and progression. Many ion channels are bona fide cellular sensors of changes in pH. Yet, the interplay between the acidic tumor microenvironment and ion channel regulation in PDAC is poorly understood. In this study, we show that acid adaption increases PANC-1 cell migration but attenuates proliferation and spheroid growth, which are restored upon recovery. Moreover, acid adaptation and recovery conditions favor the plasma membrane localization of the pH-sensitive calcium (Ca²⁺) channel transient receptor potential C1 (TRPC1), TRPC1-mediated Ca²⁺ influx, channel interaction with the PI3K p85α subunit and calmodulin (CaM), and AKT and ERK1/2 activation. Knockdown (KD) of TRPC1 suppresses cell migration, proliferation, and spheroid growth, notably in acid-recovered cells. KD of TRPC1 causes the accumulation of cells in G0/G1 and G2/M phases, along with reduced expression of CDK6, −2, and −1, and cyclin A, and increased expression of p21^CIP1. TRPC1 silencing decreases the basal Ca²⁺ influx in acid-adapted and -recovered cells, but not in normal pH conditions, and Ca²⁺ chelation reduces cell migration and proliferation solely in acid adaptation and recovery conditions. In conclusion, acid adaptation and recovery reinforce the involvement of TRPC1 in migration, proliferation, and cell cycle progression by permitting Ca²⁺ entry and forming a complex with the PI3K p85α subunit and CaM. Full article

(This article belongs to the Special Issue Regulation, Role and Targeting of Calcium Signaling Pathways in Cancer)

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Review

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22 pages, 1500 KiB

Open AccessReview

Calcium Homeostasis in the Development of Resistant Breast Tumors

by Desirée Martin-García, Teresa Téllez, Maximino Redondo and Marilina García-Aranda

Cancers 2023, 15(11), 2872; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers15112872 - 23 May 2023

Viewed by 3036

Abstract

Cancer is one of the main health problems worldwide. Only in 2020, this disease caused more than 19 million new cases and almost 10 million deaths, with breast cancer being the most diagnosed worldwide. Today, despite recent advances in breast cancer treatment, a significant percentage of patients will either not respond to therapy or will eventually experience lethal progressive disease. Recent studies highlighted the involvement of calcium in the proliferation or evasion of apoptosis in breast carcinoma cells. In this review, we provide an overview of intracellular calcium signaling and breast cancer biology. We also discuss the existing knowledge on how altered calcium homeostasis is implicated in breast cancer development, highlighting the potential utility of Ca²⁺ as a predictive and prognostic biomarker, as well as its potential for the development of new pharmacological treatments to treat the disease. Full article

(This article belongs to the Special Issue Regulation, Role and Targeting of Calcium Signaling Pathways in Cancer)

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