IndraLab

Statements


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"Consistent with our previous finding , USP35 overexpression promoted the growth of ER+ breast tumors, whereas (+)-JQ-1 inhibited the tumor growth increased by USP35 overexpression (Fig. 7B, D, E)."

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"USP35 is overexpressed in KIRC and associated with poor prognosis, likely promoting tumor progression through oncogenic pathways and immune modulation."

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"We observed that USP35 overexpression markedly promoted tumor growth and drug resistance, but depleting FUCA1 in USP35-overexpressed cells reversed the tumor growth to the basal levels, and re-sensitized the tumors to the chemo-treatments, as indicated by representative images, tumor weight and growth curve (Fig. 6A–C)."

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"We also observed that USP35 knockdown repressed the development of xenograft HCC tumors in vivo."

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"In summary, these results suggest that USP35 may promote HCC development by stabilizing ABHD17C, thereby facilitating tumor progress through the activation of the PI3K/AKT signal cascade."

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"In this study, we highlighted the SREBP2-dependent MVA crosstalk is activated by USP35/BRFP1 axis to drive tumor progression."

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"Importantly, depletion of USP35 significantly enhances the anti-tumor immunity and synergizes with oncolytic virotherapy to suppress xenograft tumor growth of melanoma cells."

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"Depletion of USP35 promotes ferroptosis and suppresses lung cancer cell growth and tumor progression [16]."

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"Through a systematic survey in the association of human ubiquitin-specific proteases with patient prognosis of renal clear cell carcinoma and subsequent phenotypic validation, we uncovered the tumor-promoting role of USP35."