Ginsenoside Rg3 suppresses the growth of gemcitabine‐resistant pancreatic cancer cells by upregulating lncRNA‐CASC2 and activating PTEN signaling

Abstract Pancreatic cancer is one of the most fatal malignancies with high mortality. Gemcitabine (GEM)‐based chemotherapy is the most important treatment. However, the development of GEM resistance leads to chemotherapy failure. Previous studies demonstrated the anticancer activity of ginsenoside Rg3 in a variety of carcinomas through modulating multiple signaling pathways. In the present study, 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl tetrazolium bromide assay, colony formation assay, flow cytometry apoptosis assay, Western blotting assay, xenograft experiment, and immunohistochemistry assay were performed in GEM‐resistant pancreatic cancer cell lines. Ginsenoside Rg3 inhibited the viability of GEM‐resistant pancreatic cancer cells in a time‐dependent and concentration‐dependent manner through induction of apoptosis. The level of long noncoding RNA cancer susceptibility candidate 2 (CASC2) and PTEN expression was upregulated by the ginsenoside Rg3 treatment, and CASC2/PTEN signaling was involved in the ginsenoside Rg3‐induced cell growth suppression and apoptosis in GEM‐resistant pancreatic cancer cells. Ginsenoside Rg3 could be an effective anticancer agent for chemoresistant pancreatic cancer.