| Literature DB >> 32368394 |
Zeng Ye1,2,3,4, Qiangsheng Hu1,2,3,4, Qifeng Zhuo1,2,3,4, Yuemeng Zhu5, Guixiong Fan1,2,3,4, Mengqi Liu1,2,3,4, Qiqing Sun1,2,3,4, Zheng Zhang1,2,3,4, Wensheng Liu1,2,3,4, Wenyan Xu1,2,3,4, Shunrong Ji1,2,3,4, Xianjun Yu1,2,3,4, Xiaowu Xu1,2,3,4, Yi Qin1,2,3,4.
Abstract
ADP Ribosylation Factor 6 (ARF6) is a part of the RAS superfamily and regulates vesicular trafficking, remodeling of membrane lipids, and signaling pathways. Our previous study has found that ARF6, functioned as a downstream of Kras/ERK signaling pathway, could promote proliferation and Warburg effect in pancreatic cancer cells. Moreover, ARF6 is promising to be a biomarker for predicting prognosis of pancreatic cancer. Ferroptosis is a new defined iron-dependent form of nonapoptotic cell death, which is closely related to Kras mutation. Therefore, it is urgent to further explore the relationship between ARF6 and ferroptosis. Our study demonstrated that ARF6 did not directly regulate lipid peroxidation, but endowed pancreatic cancer cells to a status that is sensitive to oxidative stress, especially RSL3-induced lipid peroxidation. Further study revealed that ARF6 could also regulate gemcitabine resistance via multiple pathways. In conclusion, ARF6 has a profound effect on pancreatic cancer development. AJCREntities:
Keywords: ACSL4; ARF6; Ferroptosis; gemcitabine; pancreatic cancer
Year: 2020 PMID： 32368394 PMCID： PMC7191101
Source DB: PubMed Journal: Am J Cancer Res ISSN： 2156-6976 Impact factor: 6.166