Hydrogen Sulfide Metabolism and Signaling in the Tumor Microenvironment

Advances in Experimental Medicine and Biology
Alessandro GiuffrèJoão B Vicente

Abstract

Hydrogen sulfide (H2S), while historically perceived merely as a toxicant, has progressively emerged as a key regulator of numerous processes in mammalian physiology, exerting its signaling function essentially through interaction with and/or modification of proteins, targeting mainly cysteine residues and metal centers. As a gaseous signaling molecule that freely diffuses across aqueous and hydrophobic biological milieu, it has been designated the third 'gasotransmitter' in mammalian physiology. H2S is synthesized and detoxified by specialized endogenous enzymes that operate under a tight regulation, ensuring homeostatic levels of this otherwise toxic molecule. Indeed, imbalances in H2S levels associated with dysfunctional H2S metabolism have been growingly correlated with various human pathologies, from cardiovascular and neurodegenerative diseases to cancer. Several cancer cell lines and specimens have been shown to naturally overexpress one or more of the H2S-synthesizing enzymes. The resulting increased H2S levels have been proposed to promote cancer development through the regulation of various cancer-related processes, which led to the interest in pharmacological targeting of H2S metabolism. Herein are summarized some of...Continue Reading

Citations

Sep 5, 2020·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Ana HipólitoJacinta Serpa
Feb 12, 2021·International Journal of Molecular Sciences·Franck PaganelliJean Ruf
Jan 24, 2021·Pharmacological Research : the Official Journal of the Italian Pharmacological Society·Kelly AscençãoCsaba Szabo
Nov 20, 2020·Biochimica Et Biophysica Acta. Bioenergetics·Karim ZuhraAlessandro Giuffrè
Aug 12, 2020·Pharmacological Research : the Official Journal of the Italian Pharmacological Society·Nahzli DilekCsaba Szabo
Jul 3, 2021·International Journal of Molecular Sciences·Rong-Hsuan WangKai-Ti Lin

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