Investigators discuss common adaptive signaling mechanisms against these stresses including unfolded protein responses, antioxidant response element signaling, autophagy, mitophagy, and mitochondrial fission/fusion, signaling effector stimulator of interferon genes-mediated responses, and activation of pattern recognition receptors.
Scientists determined that phosphate and tensin homology deleted on chromosome ten (PTEN) deficiency promoted protein synthesis and proteasome subunit expression and proteolytic activity, creating a dependency on the proteasome for cancer cell growth and survival.
Researchers demonstrated that tripartite motif-containing 2 (TRIM2) was expressed in a high percentage of pancreatic tumors. High TRIM2 expression was negatively correlated with the outcome of pancreatic cancer. TRIM2 silencing significantly inhibited the proliferation, migration, invasion, and in vivo tumorigenicity of pancreatic cancer cells.
Sun, Q., Ye, Z., Qin, Y., Fan, G., Ji, S., Zhuo, Q., Xu, W., Liu, W., Hu, Q., Liu, M., Zhang, Z., Xu, X., & Yu, X. (2020). Oncogenic function of TRIM2 in pancreatic cancer by activating ROS-related NRF2/ITGB7/FAK axis. Oncogene, 1–17. https://doi.org/10.1038/s41388-020-01452-3Cite