Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with limited therapeutic options and a poor prognosis. Resveratrol (RES), a natural polyphenolic compound, has demonstrated antitumor activity in multiple cancer types; however, its underlying mechanisms in pancreatic cancer remain incompletely understood. In this study, we investigated the effects of RES on pancreatic cancer cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), with a particular focus on the role of inhibitor of growth family member 5 (ING5). Pancreatic cancer cell lines PANC1 and SW1990 were treated with RES, and cell viability, clonogenic growth, migration, and invasion were assessed using CCK-8, colony formation, wound-healing, and Transwell assays, respectively. ING5 expression and localization were evaluated by immunofluorescence, RT-qPCR, and Western blotting, and its functional significance was further examined using siRNA-mediated knockdown. RES treatment significantly suppressed pancreatic cancer cell proliferation, migration, invasion, and EMT in vitro, accompanied by upregulation of ING5 expression and increased E-cadherin levels with concomitant reduction of N-cadherin expression. Silencing ING5 enhanced malignant cellular behaviors and partially reversed the inhibitory effects of RES on EMT-associated phenotypes and cell growth. These findings indicate that ING5 contributes to the antitumor effects of RES and functions as an important mediator in the suppression of pancreatic cancer progression. Collectively, our results suggest that RES restrains pancreatic cancer cell aggressiveness at least in part through upregulation of ING5, highlighting the RES-ING5 axis as a potential therapeutic target for pancreatic cancer intervention.
Wang et al. (Fri,) studied this question.