IndraLab

Statements

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"In vitro knockdown of USP35 suppresses KIRC cell proliferation, migration, and EMT."
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"Ectopic USP35 expression in cancer cells inhibited cell proliferation, while silencing USP35 induced proliferation in vitro."
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"USP35 depletion could decrease PRAD cell proliferation rates relative to parental control cells that could be restored by USP35 overexpression, as suggested by the cell viability assays (Fig. 2D)."
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"Colony formation assays revealed that silencing USP35 led to a significant decrease in the number of colonies formed by KIRC cells, indicating reduced cell proliferation (Fig. 8B)."
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"The results demonstrated that USP35 knockdown with siRNAs remarkably reduced cell proliferation and survival ability (Fig. S6 A-C), whereas overexpression of USP35 promoted cell proliferation and survival (Fig. S6 D-F), which is consistent with the findings that USP35 can promote mitotic progression 30.To further investigate whether the enzymatic activity of USP35 is required for its biological effects, we transfected GC cells with a WT-USP35 vector or USP35-C450A mutant (Fig. 5A) and performed Transwell and scratch wound healing assays."
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"Collectively, these data indicated that USP35 promotes the proliferation, migration, and stemness properties of PRAD cells both in vitro and in vivo."
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"It has been shown that USP35 overexpression enhances CRC cell proliferation and resistance to oxaliplatin and 5-FU[85]."
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"Upregulation of USP35 promotes CRC cell proliferation and imparts resistance to both oxaliplatin and 5-Fu."
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"We also verified that USP35 promotes the proliferation and survival of GC cells, which is consistent with certain findings reported previously 30."
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"Knockdown of USP35 causes reduced proliferation, cell cycle arrest, increased apoptosis, and mitigated migration and invasion of HCC cells."
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"Moreover, the density and proliferation of xenograft tumor cells were also reduced by USP35 knockdown as indicated by H&E staining and Ki-67 IHC results (Fig. 7J–L)."
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"Further functional studies showed that knockdown USP35 expression inhibited cell proliferation and promoted apoptosis."
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"Importantly, we demonstrated that PFK-1 is an essential mediator for USP35-induced cell proliferation and glycolysis in vitro and in vivo."
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"In vitro experiments demonstrate that USP35 knockdown inhibits KIRC cell proliferation and migration while modulating EMT-related protein expression, confirming its functional importance in KIRC progression."
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"USP35 promotes cell proliferation and chemotherapeutic resistance through stabilizing FUCA1 in colorectal cancer."
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"Further functional studies showed that enhanced USP35 expression promoted CRC cell proliferation and resistance to oxaliplatin (OXA) and 5-fluorouracil (5-FU), whereas USP35 depletion impeded cell proliferation and sensitized cells to OXA and 5-FU treatments."
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"Importantly, we demonstrated that FUCA1 was an essential mediator for USP35-induced cell proliferation and chemo-resistance in vitro and in vivo."
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"Therefore, we performed a series of functional studies under the regulation of USP35-FUCA1 axis, aiming to better understand the role of FUCA1 in cancers.In the present study, we first demonstrated that USP35 promoted CRC cell proliferation and resistance to the drugs (oxaliplatin and 5-fluorouracil) routinely used in the CRC clinic."
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"USP35 promotes CRC cell proliferation and chemo-resistance."
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"To investigate the possible mechanism for USP35-mediated cell proliferation and drug resistance, we transfected Flag-tagged USP35 expression plasmid into the HCT116 cell line, immunoprecipitated the USP35-associated proteins with anti-Flag antibody, separated the proteins by SDS-PAGE, and analyzed the immunoprecipitated proteins by mass spectrometry (Fig. 3A)."
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