Mitochondrial Calcium Regulation of Redox Signaling in Cancer

Céline Delierneux, Sana Kouba, Santhanam Shanmughapriya, Marie Potier-Cartereau, Mohamed Trebak, Nadine Hempel

Research output: Contribution to journalReview articlepeer-review

78 Scopus citations


Calcium (Ca2+) uptake into the mitochondria shapes cellular Ca2+ signals and acts as a key effector for ATP generation. In addition, mitochondria-derived reactive oxygen species (mROS), produced as a consequence of ATP synthesis at the electron transport chain (ETC), modulate cellular signaling pathways that contribute to many cellular processes. Cancer cells modulate mitochondrial Ca2+ ([Ca2+]m) homeostasis by altering the expression and function of mitochondrial Ca2+ channels and transporters required for the uptake and extrusion of mitochondrial Ca2+. Regulated elevations in [Ca2+]m are required for the activity of several mitochondrial enzymes, and this in turn regulates metabolic flux, mitochondrial ETC function and mROS generation. Alterations in both [Ca2+]m and mROS are hallmarks of many tumors, and elevated mROS is a known driver of pro-tumorigenic redox signaling, resulting in the activation of pathways implicated in cellular proliferation, metabolic alterations and stress-adaptations. In this review, we highlight recent studies that demonstrate the interplay between [Ca2+]m and mROS signaling in cancer.

Original languageEnglish (US)
Article number1787
Issue number2
StatePublished - Feb 12 2020

All Science Journal Classification (ASJC) codes

  • General Biochemistry, Genetics and Molecular Biology


Dive into the research topics of 'Mitochondrial Calcium Regulation of Redox Signaling in Cancer'. Together they form a unique fingerprint.

Cite this