Biochemical and biophysical research communications · 2026
DCAF13 is associated with pancreatic ductal adenocarcinoma progression and p53-related signaling in TP53-mutant cells.
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Fan Xiaofang, Zhao Hengping, Wu Bin, Lv Yichen, Chen Wei, Chen Qi, Hu Lingyu, Yu Shenjie, Wang Jiale, He Yahui, Yu Jiaqi
Аннотация
BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with poor prognosis. DDB1 and CUL4 associated factor 13 (DCAF13) has been implicated in tumor progression, but its clinical relevance and biological function in PDAC remain unclear.
METHODS: Public databases (GEPIA2 and Kaplan-Meier Plotter) were used to analyze DCAF13 expression and its prognostic value in PDAC. Tumor and paired adjacent tissues from 90 PDAC patients were examined by immunohistochemistry to assess DCAF13 protein expression and its association with clinicopathological features and survival. DCAF13 expression in HPDE6-C7, AsPC-1 and MiaPaCa-2 cells was detected by qRT-PCR and Western blotting. Gain- and loss-of-function models were established to evaluate the effects of DCAF13 on cell migration, invasion and apoptosis using wound healing, Transwell and flow cytometry assays. Changes in p53-related signaling proteins were examined by Western blot.
RESULTS: Bioinformatic analyses revealed significantly elevated DCAF13 expression in PDAC and its association with shorter overall and disease-free survival. Clinically, DCAF13 protein was overexpressed in PDAC tissues and correlated with tumor differentiation (P = 0.006). In PDAC cell lines, DCAF13 knockdown suppressed migration and invasion while promoting apoptosis in vitro, whereas DCAF13 overexpression exerted the opposite effects. In TP53-mutant PDAC cells, DCAF13 knockdown was associated with increased expression of p53-related proteins, including p53 and its downstream targets p21, BAX and FAS, suggesting a potential association between DCAF13 and altered p53-related signaling in this cellular context.
CONCLUSIONS: DCAF13 is overexpressed in PDAC and associated with poor prognosis. DCAF13 may promote malignant phenotypes in vitro and alter p53-related signaling in TP53-mutant PDAC cells. These findings suggest that DCAF13 may have potential value as a prognostic biomarker and exploratory therapeutic candidate for PDAC, although further validation in WT-p53 and in vivo models is still required.
METHODS: Public databases (GEPIA2 and Kaplan-Meier Plotter) were used to analyze DCAF13 expression and its prognostic value in PDAC. Tumor and paired adjacent tissues from 90 PDAC patients were examined by immunohistochemistry to assess DCAF13 protein expression and its association with clinicopathological features and survival. DCAF13 expression in HPDE6-C7, AsPC-1 and MiaPaCa-2 cells was detected by qRT-PCR and Western blotting. Gain- and loss-of-function models were established to evaluate the effects of DCAF13 on cell migration, invasion and apoptosis using wound healing, Transwell and flow cytometry assays. Changes in p53-related signaling proteins were examined by Western blot.
RESULTS: Bioinformatic analyses revealed significantly elevated DCAF13 expression in PDAC and its association with shorter overall and disease-free survival. Clinically, DCAF13 protein was overexpressed in PDAC tissues and correlated with tumor differentiation (P = 0.006). In PDAC cell lines, DCAF13 knockdown suppressed migration and invasion while promoting apoptosis in vitro, whereas DCAF13 overexpression exerted the opposite effects. In TP53-mutant PDAC cells, DCAF13 knockdown was associated with increased expression of p53-related proteins, including p53 and its downstream targets p21, BAX and FAS, suggesting a potential association between DCAF13 and altered p53-related signaling in this cellular context.
CONCLUSIONS: DCAF13 is overexpressed in PDAC and associated with poor prognosis. DCAF13 may promote malignant phenotypes in vitro and alter p53-related signaling in TP53-mutant PDAC cells. These findings suggest that DCAF13 may have potential value as a prognostic biomarker and exploratory therapeutic candidate for PDAC, although further validation in WT-p53 and in vivo models is still required.