Project description:The mechanism underlying the loss of normal liver tissues in liver cirrhosis, mainly hepatocytes, is not well-characterized. Endoplasmic reticulum (ER) stress-induced cell death has emerged as a potential mechanism for chronic liver diseases. We have previously demonstrated that cyclooxygenase-2 (COX-2) is closely related to the progress of liver cirrhosis. In this study, we aimed to verify whether hepatocytes COX-2 deficiency could protect liver injury via inducing ER stress in liver cirrhosis.
Project description:S4, a sulfonamide drug, has been confirmed to induce apoptosis and autophagy in cancer cells. Immunogenic cell death is a special cell death type which is closely related to apoptosis and autophagy. We performed RNA-seq to determine the impact of S4 on global gene expression profile in LN229 cells. Our results show that S4 induces immunogenic cell death via the response to endoplasmic reticulum stress.
Project description:We tracked the gene expression events following treatment of maize seedlings with the endoplasmic reticulum (ER) stress agent tunicamycin. ER stress elicits the unfolded protein response (UPR) and when plants are faced with persistent stress, the UPR transitions from an adaptive or cell survival phase to programmed cell death.
Project description:Protein homeostasis in the endoplasmic reticulum (ER) has recently emerged as a therapeutic target for cancer treatment. Disruption of ER homeostasis results in ER stress, which is a major cause of cell death for cells exposed to the proteasome inhibitor Bortezomib, an anti-cancer drug approved for treatment of multiple myeloma and Mantle cell lymphoma. We recently reported that the ERAD inhibitor Eeyarestatin I (EerI) also disturbs ER homeostasis and has anti-cancer activities resembling that of Bortezomib. Our findings reveal a class of bifunctional chemical agents that can preferentially inhibit membrane-bound p97 to disrupt ER homeostasis and induce tumor cell death. These results also suggest that the AAA ATPase p97 may be a potential drug target for cancer therapy. Cells were treated with EerI, CBU-028, or 5-NA each at 10uM in duplicates for 10h
