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- W4366996027 abstract "Gemcitabine is the first-line drug for chemotherapy of pancreatic cancer. However, owing to the inherent and acquired resistance, gemcitabine does not change obviously the prognosis of patients with pancreatic cancer. Exploration of the mechanism of acquired resistance to gemcitabine is of great clinical importance.Human gemcitabine-resistant pancreatic cancer cells were established and GAS5 expression levels were determined. Proliferation and apoptosis were detected in vitro. Multidrug resistance related proteins were determined by western blotting. The relationship between GAS5 and miR-21 were evaluated by luciferase reporter assay.The results showed that GAS5 was significantly downregulated in gemcitabine-resistant PAN-1 and CaPa-2 cells. Overexpression of GAS5 in gemcitabine-resistant PAN-1 and CaPa-2 cells significantly inhibited cell proliferation, induced cell apoptosis and reduced MRP1, MDR1, and ABCG2 expressions. In addition, miR-21 mimics reversed the phenotype of GAS5-overexpression in gemcitabine-resistant PAN-1 and CaPa-2 cells.Taken together, GAS5 was involved in gemcitabine resistance in pancreatic carcinoma and possibly through regulating miR-21, and subsequent cell proliferation, apoptosis and expression of multidrug resistant transporters." @default.
- W4366996027 created "2023-04-27" @default.
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- W4366996027 date "2023-03-01" @default.
- W4366996027 modified "2023-10-18" @default.
- W4366996027 title "LncRNA GAS5 Regulates Gemcitabine Resistance in Pancreatic Carcinoma by Targeting miRNA-21." @default.
- W4366996027 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37094852" @default.
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