Study summary · research use only
Mitochondrial-Derived Peptide MOTS-c Suppresses Ovarian Cancer Progression by Attenuating USP7-Mediated LARS1 Deubiquitination
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This laboratory study (species not specified) investigated the mitochondrial-derived peptide MOTS-c in ovarian cancer (OC). MOTS-c levels were reported to be reduced in serum and tumor tissue from OC patients and associated with poorer prognosis. In OC cells, exogenous MOTS-c was reported to inhibit proliferation, migration, and invasion, and to induce cell cycle arrest and apoptosis. Mechanistically, the abstract reports that MOTS-c interacts with LARS1 and promotes its ubiquitination and degradation by competing with the deubiquitinase USP7 for LARS1 binding, and that LARS1 was increased and had an oncogenic role in OC. In vivo, MOTS-c was reported to show an anti-tumor effect on OC growth without systemic toxicity.
Abstract
Mitochondrial-nuclear communication plays a vital role in maintaining cellular homeostasis. MOTS-c, a short peptide derived from the 12S rRNA of mitochondrial DNA, has been suggested as a retrograde mitochondrial signal. Although recent clinical studies have suggested a possible link between MOTS-c and human cancer, the role of MOTS-c in tumorigenesis has yet to be investigated. Here, MOTS-c levels are found to be reduced in both serum and tumor tissues from ovarian cancer (OC) patients, which are associated with poor patients' prognosis. Exogenous MOTS-c inhibits the proliferation, migration and invasion of OC cells, and induces cell cycle arrest and apoptosis. Mechanistically, MOTS-c interacts with LARS1 and promotes its ubiquitination and proteasomal degradation. In addition, USP7 was identified as a deubiquitinase of LARS1, and MOTS-c can attenuates USP7-mediated LARS1 deubiquitination by competing with USP7 for binding to LARS1. Besides, LARS1 was found to be increased and play an important oncogenic function in OC. More importantly, MOTS-c displays a marked anti-tumor effect on OC growth without systemic toxicity in vivo. In conclusion, this study reveals a crucial role of MOTS-c in OC and provides a possibility for MOTS-c as a therapeutic target for the treatment of this manlignacy.
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