ArticleTranslational oncology2026
MAZ-Mediated ubiquitin-conjugating enzyme E2C upregulation promotes breast cancer progression via the MAPK signaling pathway.
Article in Translational oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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7 authors.
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Abstract
backgroundMalignant proliferation and invasion of tumor cells are the primary causes of death among patients with breast cancer, yet the molecular mechanisms orchestrating cancer metastasis are not well elucidated. Ubiquitin-conjugating enzyme E2C (UBE2C) has been reported to be involved in the tumorigenesis and development of various malignant tumors; however, the biological roles and underlying mechanisms of UBE2C in breast cancer remain unclear.
methodsUBE2C expression was analyzed in breast cancer tissue and cell lines using immunohistochemistry, quantitative reverse transcription PCR (RT-qPCR) and Western blot. The biological roles of UBE2C and its transcription factor MAZ were investigated in vitro using CCK-8, plate cloning, scratch, Transwell, cell cycle and apoptosis assays, while a nude mouse subcutaneous tumorigenic model was employed for the in vivo studies. Dual-luciferase reporter assay and chromatin immunoprecipitation (ChIP) assay were conducted to validate the binding relationship between MAZ and UBE2C.
resultsUBE2C expression is elevated in breast cancer, and higher levels of UBE2C are associated with poorer survival among patients with breast cancer. UBE2C promotes the progression of breast cancer both in vivo and in vitro. Additionally, UBE2C is a direct transcriptional target of MAZ, which also accelerates malignant development of breast cancer. Furthermore, UBE2C exerts its oncogenic effects dependent on the MAPK signaling pathway.
conclusionOur findings highlight the critical role of the MAZ/UBE2C/MAPK signaling axis in the progression of breast cancer and identify potential novel therapeutic targets for its treatment.
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