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USP35 activates HYCC1. 12 / 12
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"Moreover, USP35 knockdown impaired the migration and invasion capabilities of HCC cells (Fig. 3L–O)."
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"USP35 deficiency suppresses HCC development in vivo."
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"Together, these data suggest that USP35 promotes HCC development in vivo."
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"Our data also demonstrate that USP35 promotes HCC development by stabilizing ABHD17C and activates the PI3K/AKT pathway.The oncogenic function of USP35 in other cancers has been well characterized."
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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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"Given the diversity of its substrates, it will be important to investigate whether USP35 promotes HCC development by additional targets other than ABHD17C.ABHD17 depalmitoylases can regulate palmitoylation of N-RAS to change its subcellular localization, and selective inhibitor of ABHD17 proteins is reported to repress N-RAS signaling and impair acute myeloid leukemia cell growth [15, 16]."
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"In line with these reports, we found that the PI3K/AKT pathway is disrupted in USP53-deficient HCC cells, which is likely caused by a lack of sufficient ABHD17C.In conclusion, our study provides evidence that USP35 promotes HCC development by stabilizing ABHD17C (Fig. 8)."
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"USP35 promotes HCC development by stabilizing ABHD17C and activating the PI3K/AKT signaling pathway."
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"In support of these in vitro observations, xenograft assay data also showed that USP35 deficiency repressed HCC development in vivo, characterized by reduced proliferation and disrupted PI3K/AKT signaling."
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"As patients with HCC with liver cancer nodules >3 were not included in the study, this is a deficiency of the present study.In conclusion, the results of the present study demonstrated that USP35 was significantly elevated in HCC."
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"Together, these findings demonstrate that USP35 may promote HCC development by stabilization of ABHD17C and activation of the PI3K/AKT pathway."
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