IndraLab

Statements



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"Overexpression of BRCC3 Increased Cell Proliferation and Migration."

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"Furthermore, BRCC36 promoted cell proliferation, migration, and invasion, while inhibiting ferroptosis and inducing pyroptosis in liver cancer cells."

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"Additionally, BRCC36 regulates HMGCR deubiquitination, and inhibiting BRCC36 can suppress liver cancer cell proliferation [9]."

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"Moreover, mRNA expression profiling of BRCC3 has been reported in human breast cancer cells, and exogenous BRCC3 expression is associated with delayed death and increased breast cancer cell proliferation [32]."

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"Moreover, as an oncogene in hepatocellular carcinoma (HCC), BRCC36 promoted cancer cell proliferation, migration, invasion, and tumor growth."

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"We investigated the regulatory roles of BRCC36 in Met-stimulated milk lipid and protein synthesis, cell proliferation, and the mTOR signaling pathway."

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"Consistently, treatment with thiolutin, an inhibitor of BRCC36, specifically suppressed cell proliferation and induced cell apoptosis in ITD cells."

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"In conclusion, BRCC3 promotes TNBC cell proliferation and metastasis by increasing the stability of ZEB1 under pathological conditions."

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"Tao et al. (21) reported that BRCC3 enhanced cell proliferation and migration by activating TRAF2/NF-κB pathway."

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"In this study, we observed that thiolutin, an inhibitor of BRCC36, 37 reduced the level of p‐STAT5, impaired cell proliferation, and promoted apoptosis in ITD cells such as MV4‐11 cells."

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"Besides, BRCC3 could activate NLRP3 inflammasome-dependent pyroptosis (26), which could then promote tumor progression.In conclusion, UCA1 acted as an oncogene in pancreatic cancer by partly regulating miR-582-5p/BRCC3, which promoted cell proliferation, migration, and inhibited apoptosis."

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"The deubiquitinase BRCC3 increases the stability of ZEB1 and promotes the proliferation and metastasis of triple-negative breast cancer cells."

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"The comprehensive analysis of the functions of BRCC3, an E3 ubiquitin ligase associated with heightened cell proliferation, ANP32E, which regulates histones, aids in cell adhesion, and promotes the proliferation of TNBC cells, and ANLN, which facilitates cytokinesis and encourages tumor cell proliferation, highlights the critical importance of these genes in the progression of TNBC and establishes them as prospective therapeutic targets."