Article Publish Status: FREE
Abstract Title:

Mitochondria-targeted magnolol inhibits OXPHOS, proliferation, and tumor growth via modulation of energetics and autophagy in melanoma cells.

Abstract Source:

Cancer Treat Res Commun. 2020 Sep 17 ;25:100210. Epub 2020 Sep 17. PMID: 32987287

Abstract Author(s):

Gang Cheng, Micael Hardy, Jacek Zielonka, Katherine Weh, Monika Zielonka, Kathleen A Boyle, Mahmoud Abu Eid, Donna McAllister, Brian Bennett, Laura A Kresty, Michael B Dwinell, Balaraman Kalyanaraman

Article Affiliation:

Gang Cheng


INTRODUCTION: Melanoma is an aggressive form of skin cancer for which there are no effective drugs for prolonged treatment. The existing kinase inhibitor antiglycolytic drugs (B-Raf serine/threonine kinase or BRAF inhibitors) are effective for a short time followed by a rapid onset of drug resistance.

PRESENTATION OF CASE: Here, we show that a mitochondria-targeted analog of magnolol, Mito-magnolol (Mito-MGN), inhibits oxidative phosphorylation (OXPHOS) and proliferation of melanoma cells more potently than untargeted magnolol. Mito-MGN also inhibited tumor growth in murine melanoma xenografts. Mito-MGN decreased mitochondrial membrane potential and modulated energetic and mitophagy signaling proteins.

DISCUSSION: Results indicate that Mito-MGN is significantly more potent than the FDA-approved OXPHOS inhibitor in inhibiting proliferation of melanoma cells.

CONCLUSION: These findings have implications in the treatment of melanomas with enhanced OXPHOS status due to metabolic reprogramming or drug resistance.

Study Type : In Vitro Study

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