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UBE2C promotes pancreatic cancer progression through PI3K/Akt/mTOR signaling pathway
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DOI：10.1080/15384101.2026.2668450.png)
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Abstract
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UBE2C, a key member of the ubiquitin-proteasome system, is overexpressed in various malignant tumors and correlates with poor prognosis. Our findings reveal that UBE2C expression is elevated in both pancreatic cancer cell lines and tissues compared to normal pancreatic cells and tissues, with this aberrant expression linked to a poor prognosis. Knockdown of UBE2C expression reduces pancreatic cancer cell proliferation, migration, and invasion, while significantly decreasing the phosphorylation of the PI3K/AKT/mTOR signaling pathway. Administration of the pathway activator SC79 reverses the inhibitory effects of UBE2C knockdown on the PI3K/AKT/mTOR pathway, restoring the proliferation, migration, and invasion of pancreatic cancer cells. These results suggest that UBE2C promotes pancreatic cancer progression via the PI3K/AKT/mTOR signaling pathway. Thus, UBE2C serves as a potential biomarker for the early detection and diagnosis of pancreatic cancer and may represent a promising therapeutic target.
Keywords:
UBE2C
pancreatic cancer
PI3K
AKT
mTOR
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