Yongfei Yang

Prof. Yongfei Yang

China University of Petroleum (East China)
orcid

Research Focus & Metrics

Academic Career Length

19Years (2008-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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18 January 2018 in Cell Death & Differentiation
Verified
Journal Article
Open access
PDF file
MLMeiying Luo
Meiying Luo
LWLongfei Wu
Longfei Wu
KZKexin Zhang
Kexin Zhang
HWHong Wang
Hong Wang
TZTian Zhang
Tian Zhang
YYYongfei Yang
Yongfei Yang
Ferroptosis is a regulated form of cell death driven by small molecules or conditions that induce lipid-based reactive oxygen species (ROS) accumulation. This form of iron-dependent cell death is morphologically and genetically distinct from apoptosis, necroptosis, and autophagy. miRNAs are known to play crucial roles in diverse fundamental biological processes. However, to date no study has reported miRNA-mediated regulation of ferroptosis. Here we show that miR-137 negatively regulates ferroptosis by directly targeting glutamine transporter SLC1A5 in melanoma cells. Ectopic expression of miR-137 suppressed SLC1A5, resulting in decreased glutamine uptake and malondialdehyde (MDA) accumulation. Meanwhile, antagomir-mediated inactivation of endogenous miR-137 increased the sensitivity of melanoma cells to erastin- and RSL3-induced ferroptosis. Importantly, knockdown of miR-137 increased the antitumor activity of erastin by enhancing ferroptosis both in vitro and in vivo. Collectively, these data indicate that miR-137 plays a novel and indispensable role in ferroptosis by inhibiting glutaminolysis and suggest a potential therapeutic approach for melanoma.

23 January 2020 in Nature Communications
Verified
Journal Article
Open access
PDF file
YYYongfei Yang
Yongfei Yang
MLMeiying Luo
Meiying Luo
KZKexin Zhang
Kexin Zhang
JZJun Zhang
Jun Zhang
TGTongtong Gao
Tongtong Gao
WCWei Chen
Wei Chen
Ferroptosis is a newly defined form of regulated cell death characterized by the iron-dependent accumulation of lipid hydroperoxides. Erastin, the ferroptosis activator, binds to voltage-dependent anion channels VDAC2 and VDCA3, but treatment with erastin can result in the degradation of the channels. Here, the authors show that Nedd4 is induced following erastin treatment, which leads to the ubiquitination and subsequent degradation of the channels. Depletion of Nedd4 limits the protein degradation of VDAC2/3, which increases the sensitivity of cancer cells to erastin. By understanding the molecular mechanism of erastin-induced cellular resistance, we can discover how cells adapt to new molecules to maintain homeostasis. Furthermore, erastin-induced resistance mediated by FOXM1-Nedd4-VDAC2/3 negative feedback loop provides an initial framework for creating avenues to overcome the drug resistance of ferroptosis activators.

1 May 2020 in Chemical Engineering Journal
Verified
Journal Article
Closed access
Yongfei YangYongfei Yang
Yongfei Yang
JLJie Liu
Jie Liu
JYJun Yao
Jun Yao
JKJianlong Kou
Jianlong Kou
ZLZheng LI
Zheng LI
HSHai Sun
Hai Sun

1 November 2015 in Journal of Natural Gas Science and Engineering
Verified
Journal Article
Closed access
Yongfei YangYongfei Yang
Yongfei Yang
JYJun Yao
Jun Yao
CWChenchen Wang
Chenchen Wang
YGYing Gao
Ying Gao
QZQi Zhang
Qi Zhang
WSWenhui Song
Wenhui Song

1 October 2016 in Fuel
Verified
Journal Article
Closed access
WSWenhui Song
Wenhui Song
JYJun Yao
Jun Yao
YLYang Li
Yang Li
Hai SunHai Sun
Hai Sun
LZLei Zhang
Lei Zhang
HSHongguang Sui
Hongguang Sui

1 September 2019 in Fuel
Verified
Journal Article
Closed access
Yongfei YangYongfei Yang
Yongfei Yang
KWKe Wang
Ke Wang
LZLei Zhang
Lei Zhang
HSHai Sun
Hai Sun
KZKai Zhang
Kai Zhang
JMJingsheng Ma
Jingsheng Ma