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FUCA1 binds USP35. 24 / 28
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"Finally, we observed that nucleotide excision repair (NER) components (e.g., XPC, XPA, ERCC1) were up-regulated by USP35-FUCA1 axis, indicating a potential mechanism for USP35-FUCA1-mediated platinum resistance in CRC."
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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."
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"Finally, we suggested that USP35-FUCA1 axis up-regulated nucleotide excision repair (NER) components (e.g., XPC, XPA, ERCC1), which could be a potential mechanism for platinum resistance in CRC."
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"To validate our screened results, we first examined whether the physical interaction existed between USP35 and FUCA1."
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"As illustrated in Fig. xref , USP35 interacted with FUCA1 in a reciprocal fashion."
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"The interaction between endogenous USP35 and FUCA1 was also detected in LoVo and DLD-1 cells (Fig. xref )."
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"As p53 mutation was found in approximately 60% of the CRC patients [ xref ], we specifically focused on exploring the role of USP35-FUCA1 axis in p53 mutant DLD-1 and HT29 cells."
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"To explore the role of USP35-FUCA1 axis in vivo, we subcutaneously inoculated the control (EV + shNC), USP35-overexpressed (USP35 + shNC), and USP35 overexpressed FUCA1-depleted (USP35 + shFUCA1-4) HT29 cells in the athymic nude mice, intraperitoneally injected water (H 2 O), single drug (OXA as a representative), or combined drugs (OXA + 5-FU) weekly into the mice, and routinely monitored the tumor growth."
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"Next, we examined the USP35-FUCA1 axis in the human CRC tissues."
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"Therefore, these results suggest that USP35 expression correlates well with FUCA1 expression in CRC patient samples, and USP35-FUCA1 axis contributes to CRC tumor growth and chemo-resistance in vivo."
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"USP35-FUCA1 axis up-regulates nucleotide excision repair in CRC."
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"Strikingly, we found that XPA silencing partially rescue the phenotype, reinforcing the possibility that USP35-FUCA1 axis controls chemo-resistance by regulating the expression of NER components (Fig. xref )."
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"However, the detailed mechanism how USP35-FUCA1 regulates the NER warrants further investigation."
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"Hence, our current results indicate that USP35-FUCA1 axis up-regulates NER in CRC cells, which may be a possible mechanism for USP35-FUCA1-mediated oxaliplatin resistance in CRC."
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"Experiments detecting the change of autophagic flux and autophagic cell death will be of great help in further understanding the roles and mechanisms of USP35-FUCA1 axis in CRC."
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"In searching for the potential mechanism of how USP35–FUCA1 axis contributes to oxaliplatin resistance in CRC, we examined the expression of the main DNA repair pathway for platinum-induced DNA damage response (DDR)—the nucleotide excision repair (NER)."
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"We found that NER components (e.g., XPC, XPA and ERCC1) was up-regulated by the USP35-FUCA1 axis and we considered it an underlying mechanism for USP35-FUCA1 axis-mediated oxaliplatin resistance in CRC."
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"Nevertheless, whether USP35-FUCA1 axis promotes the expression of NER components at transcriptional levels, post-transcriptional modifications, translational levels, or post-translational modifications, warrants further investigation."
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"Although our study has demonstrated that USP35–FUCA1 axis confers resistance to 5-FU in CRC, we did not go further to explore the underlying mechanism."
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"Given the enzymatic activity of USP35 and FUCA1, we provide an outlook that targeting USP35–FUCA1 axis could be a plausible strategy for restricting tumor growth and chemo-resistance in CRC."
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"Further investigations demonstrated that USP35 directly targets α-L-fucosidase 1 (FUCA1) for deubiquitination, and the USP35-FUCA1 axis elevates nucleotide excision repair (NER) components, culminating in platinum resistance [ xref ]."
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"The interaction between endogenous USP35 and FUCA1 was also detected in LoVo and DLD-1 cells (Fig. 3E, F)."
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"Moreover, we checked the interaction of endogenous USP35 and FUCA1 in CRC cells using proximity ligation assay (PLA)."
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"The specific positive signals (shown in red) were observed in the cells, further indicating the physical association between USP35 and FUCA1 (Fig. 3G, H)."
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