Cannabigerol Induces Endoplasmic Reticulum Stress-Mediated Apoptosis and Ferroptosis via the IRE1α-XBP1 Axis in Human Pancreatic Cancer Cells - PubMed
5 hours ago
- #Pancreatic Cancer
- #ER Stress
- #Cannabigerol
- Cannabigerol (CBG), a non-psychoactive cannabinoid, shows anticancer properties in pancreatic cancer cells.
- CBG induces G1 cell cycle arrest and promotes apoptosis and ferroptosis in pancreatic cancer cells.
- Transcriptomic analysis shows CBG modulates gene networks related to apoptosis and ferroptosis.
- CBG upregulates apoptosis-associated proteins like cleaved caspase-3, caspase-9, and PARP1.
- CBG activates the unfolded protein response (UPR) and endoplasmic reticulum (ER) stress pathways.
- The IRE1α-XBP1 axis, a key UPR branch, is activated by CBG, leading to cytotoxicity.
- Inhibition of IRE1α reduces CBG-induced cell death, confirming ER stress's role in CBG's mechanism.
- CBG modulates ferroptosis-related genes (DDIT3, NFE2L2, HMOX1) and proteins (CHOP, NRF2, HO-1).
- CBG's dual induction of apoptosis and ferroptosis via ER stress supports its therapeutic potential in pancreatic cancer.