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Anti-Cancer Agents in Proliferation and Cell Death: The Calcium Connection

E. Varghese, SM. Samuel, Z. Sadiq, P. Kubatka, A. Liskova, J. Benacka, P. Pazinka, P. Kruzliak, D. Büsselberg,

. 2019 ; 20 (12) : . [pub] 20190620

Language English Country Switzerland

Document type Journal Article, Review

Persistent link   https://www.medvik.cz/link/bmc19044738

Calcium (Ca2+) signaling and the modulation of intracellular calcium ([Ca2+]i) levels play critical roles in several key processes that regulate cellular survival, growth, differentiation, metabolism, and death in normal cells. On the other hand, aberrant Ca2+-signaling and loss of [Ca2+]i homeostasis contributes to tumor initiation proliferation, angiogenesis, and other key processes that support tumor progression in several different cancers. Currently, chemically and functionally distinct drugs are used as chemotherapeutic agents in the treatment and management of cancer among which certain anti-cancer drugs reportedly suppress pro-survival signals and activate pro-apoptotic signaling through modulation of Ca2+-signaling-dependent mechanisms. Most importantly, the modulation of [Ca2+]i levels via the endoplasmic reticulum-mitochondrial axis and corresponding action of channels and pumps within the plasma membrane play an important role in the survival and death of cancer cells. The endoplasmic reticulum-mitochondrial axis is of prime importance when considering Ca2+-signaling-dependent anti-cancer drug targets. This review discusses how calcium signaling is targeted by anti-cancer drugs and highlights the role of calcium signaling in epigenetic modification and the Warburg effect in tumorigenesis.

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$a Varghese, Elizabeth $u Department of Physiology and Biophysics, Weill Cornell Medicine-Qatar, Education City, Qatar Foundation, Doha P.O. Box 24144, Qatar. elv2007@qatar-med.cornell.edu.
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$a Calcium (Ca2+) signaling and the modulation of intracellular calcium ([Ca2+]i) levels play critical roles in several key processes that regulate cellular survival, growth, differentiation, metabolism, and death in normal cells. On the other hand, aberrant Ca2+-signaling and loss of [Ca2+]i homeostasis contributes to tumor initiation proliferation, angiogenesis, and other key processes that support tumor progression in several different cancers. Currently, chemically and functionally distinct drugs are used as chemotherapeutic agents in the treatment and management of cancer among which certain anti-cancer drugs reportedly suppress pro-survival signals and activate pro-apoptotic signaling through modulation of Ca2+-signaling-dependent mechanisms. Most importantly, the modulation of [Ca2+]i levels via the endoplasmic reticulum-mitochondrial axis and corresponding action of channels and pumps within the plasma membrane play an important role in the survival and death of cancer cells. The endoplasmic reticulum-mitochondrial axis is of prime importance when considering Ca2+-signaling-dependent anti-cancer drug targets. This review discusses how calcium signaling is targeted by anti-cancer drugs and highlights the role of calcium signaling in epigenetic modification and the Warburg effect in tumorigenesis.
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$a Samuel, Samson Mathews $u Department of Physiology and Biophysics, Weill Cornell Medicine-Qatar, Education City, Qatar Foundation, Doha P.O. Box 24144, Qatar. sms2016@qatar-med.cornell.edu.
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$a Sadiq, Zuhair $u Department of Physiology and Biophysics, Weill Cornell Medicine-Qatar, Education City, Qatar Foundation, Doha P.O. Box 24144, Qatar. zuhairsadiq2018@u.northwestern.edu.
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$a Kubatka, Peter $u Department of Medical Biology and Department of Experimental Carcinogenesis, Division of Oncology, Biomedical Center Martin, Jessenius Faculty of Medicine, Comenius University in Bratislava, 036 01 Martin, Slovakia. kubatka@jfmed.uniba.sk.
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$a Liskova, Alena $u Department of Obstetrics and Gynecology, Jessenius Faculty of Medicine, Comenius University in Bratislava, 036 01 Martin, Slovakia. alenka.liskova@gmail.com.
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$a Benacka, Jozef $u Faculty Health and Social Work, Trnava University, 918 43 Trnava, Slovakia. jozef.benacka@centrum.cz.
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$a Pazinka, Peter $u Department of Surgery, Faculty of Medicine, Pavol Jozef Safarik University and Louise Pasteur University Hospital, 04022 Kosice, Slovakia. peter.pazinka@seznam.cz.
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$a Kruzliak, Peter $u Department of Internal Medicine, Brothers of Mercy Hospital, Polni 553/3, 63900 Brno, Czech Republic. peter.kruzliak@savba.sk. 2nd Department of Surgery, Faculty of Medicine, Masaryk University and St. Anne's University Hospital, 65692 Brno, Czech Republic. peter.kruzliak@savba.sk.
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$a Büsselberg, Dietrich $u Department of Physiology and Biophysics, Weill Cornell Medicine-Qatar, Education City, Qatar Foundation, Doha P.O. Box 24144, Qatar. dib2015@qatar-med.cornell.edu.
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