Gemcitabine in combination with epibrassinolide enhanced the apoptotic response in an ER stress-dependent manner and reduced the epithelial-mesenchymal transition in pancreatic cancer cells

Gemcitabine is a broad-spectrum antimetabolite and deoxycytidine analog recognized as standard therapy alone or in combination with other antineoplastic agents the of pancreas cancer. Drug resistance following gemcitabine treatment common phenomenon; therefore, combinational models are usually preferred. Pancreatic ductal adenocarcinoma, cancer, fourth leading cause cancer-related deaths worldwide. With increasing incidence pancreatic cancer every year, mortality rate also rising significantly because late diagnosis, limited chemotherapy options. Adjuvant after surgical resection typical option for early Mostly, 5-fluorouracil/leucovorin irinotecan oxaliplatin (FOLFIRINOX) gemcitabine/nab-paclitaxel used prognosis advanced cancer; however, chemoresistance occurs limiting effectiveness chemotherapy. Therefore, most studies focused on drugs to overcome situation. As an apoptotic agent member brassinosteroids, epibrassinolide (EBR) induces endoplasmic reticulum (ER) stress-dependent cell death different cells, shown by our group. In this study, we aimed enhance effect EBR combined cells. reduced viability inhibited proliferation PANC-1, MIA PaCa-2, AsPC-1 Each gave responses aggressiveness. However, induced apoptosis through ROS generation, which was associated ER stress PANC-1 PaCa-2 each line; led further induction line. addition, decreased N-cadherin vimentin expressions, suggesting that epithelial-mesenchymal transition cells reduced. conclusion, had therapeutic potential avoid gemcitabine-induced side effects during