AI Article Synopsis
- Pancreatic ductal adenocarcinoma (PDAC) shows poor response to gemcitabine, a common chemotherapy, with stanniocalcin-1 (STC1) identified as a gene linked to resistance.
- Research used methods like RT-qPCR and Western blot to study STC1's role in PDAC, revealing that it mediates chemoresistance through HIF-1α and activates the PI3K/AKT signaling pathway.
- Analysis indicated that high STC1 levels are associated with worse outcomes in patients treated with gemcitabine after surgery, suggesting STC1 could be a potential prognostic marker and treatment target for PDAC.
Article Abstract
Pancreatic ductal adenocarcinoma (PDAC) has a poor response to the first-line chemotherapy drug gemcitabine. We previously identified stanniocalcin-1 as a gemcitabine-resistant-related gene, but its specific role and function in pancreatic cancer remain unclear. RT-qPCR and Western blot were used to evaluate differential protein and mRNA expressions. The biological functions of genes were determined using proliferation and drug-resistance experiments. Subcutaneous tumorigenesis experiment was performed on nude mice. Prognostic analysis was performed using public databases and our clinical data. We found HIF-1α-regulated STC1 expression mediated chemoresistance in pancreatic cancer. Deeper, we explored the action mechanism of STC1 and identified PI3K/AKT as the downstream signaling pathway of STC1. Furthermore, we analyzed clinical data and found that STC1 expression was related to the prognosis of gemcitabine-treated patients after surgery. In general, we proved the HIF-1α/STC1/PI3K-AKT axis participated in PDAC progression and chemoresistance, and STC1 may serve as a potential prognostic factor and therapeutic target for PDAC treatment.
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