IndraLab

Statements

SUFU binds BAP1. 17 / 17
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"Furthermore, transcriptomic analyses and rescue experiments were performed to investigate the downstream regulatory mechanisms of the BAP1-SUFU axis in CRC cell proliferation."
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"Together, these findings highlight the therapeutic relevance of the BAP1-SUFU axis in CRC and suggest that targeting BAP1 may impair tumor growth by destabilizing SUFU."
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"Targeting the BAP1-SUFU regulatory axis as a therapeutic strategy in colorectal cancer."
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"Collectively, these findings demonstrate that the BAP1-SUFU axis drives colorectal cancer progression in vivo and establish this regulatory pathway as a promising therapeutic target, with BAP1 inhibition exerting strong anti-tumor efficacy."
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"Since canonical Hh signaling did not account for the phenotypes induced by SUFU manipulation, we next sought to identify the downstream mechanisms through which the BAP1-SUFU axis drives oncogenic behavior in CRC."
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"Together, these results indicate that BAP1 interacts with SUFU in the cytoplasm and stabilizes it by reducing ubiquitination."
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"To further investigate the role of the BAP1-SUFU axis impact in regulating proliferation-related genes, we conducted transcriptomic analysis following BAP1 knockdown combined with SUFU overexpression."
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"Transcriptomic and mechanistic analyses revealed that disruption of the BAP1-SUFU axis alters cell-cycle transcriptional programs through a Hh-independent mechanism and implicates E2F1 as a downstream regulator, which was confirmed by Western blot and rescue experiments demonstrating its essential role in driving the proliferative phenotype."
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"Having established the cellular and molecular roles of the BAP1-SUFU axis, we next interrogated its tumorigenic potential in vivo."
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"Overall, these findings suggest that the BAP1-SUFU axis regulates CRC transcriptional output through cell-cycle and replication pathways, independent of Hedgehog signaling."
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"Targeting the BAP1-SUFU axis regulate colorectal cancer growth."
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"To refine this pathway-level insight, GSEA analysis further identified E2F signaling as the primary pathway regulated by the BAP1-SUFU axis (Fig.  xref I)."
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"Functional assays, including CCK-8 cell proliferation assays and xenograft tumor models, were conducted to evaluate the biological impact of BAP1-SUFU signaling."
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"Functionally, the BAP1-SUFU complex is essential for CRC cell proliferation by regulating E2F1, a master driver of G1/S progression, through a Hedgehog-independent mechanism."
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"BAP1 interacts with SUFU and modulates its ubiquitination."
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"These results demonstrate that the BAP1-SUFU axis functions as a key upstream regulator of E2F-driven transcriptional programs in CRC, independent of canonical Hh signaling."
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"IHC analysis of excised tumors further showed markedly reduced E2F1 protein levels following BAP1 knockdown, SUFU knockdown, or pharmacological BAP1 inhibition (Fig.  xref K), reinforcing E2F1 as a key downstream effector of the BAP1-SUFU axis."
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