ArticleOncogene2026
MCCC2 stabilizes LTBP1 via suppressing SMURF1-dependent ubiquitination to drive bone metastasis in prostate cancer.
Article in Oncogene, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Prostate cancer (PCa) is one of the most common malignancies in men globally, with bone metastasis being a leading cause of death in advanced disease. Emerging evidence links methylcrotonyl-CoA carboxylase subunit 2 (MCCC2) to the migratory and invasive capacities of PCa cells, but its regulatory mechanisms in bone metastasis and therapeutic potential remain unclear. Here, liquid chromatography-mass spectrometry identified LTBP1 as a direct interacting partner of MCCC2, validated by co-immunoprecipitation and GST pulldown assays. Functional studies demonstrated that MCCC2 promotes PCa cell migration, invasion in vitro, and bone metastasis in vivo. Mechanistically, MCCC2 competitively inhibits SMURF1-mediated ubiquitination and degradation of LTBP1, stabilizing LTBP1 to activate TGF-β signaling. Clinically, high MCCC2 expression correlates with elevated LTBP1 levels, increased bone metastasis incidence, and poor prognosis in PCa patients. These findings reveal that MCCC2 drives PCa bone metastasis via the LTBP1-TGF-β axis, highlighting MCCC2 as a promising therapeutic target for preventing or treating bone metastasis.
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