A5058521863- Ferroptosis and cancer prognosis
- RNA modifications and cancer
- International Arbitration and Investment Law
- Cancer, Hypoxia, and Metabolism
- World Trade Organization Law
- Epigenetics and DNA Methylation
- Cancer-related molecular mechanisms research
- MicroRNA in disease regulation
- Pluripotent Stem Cells Research
- Cancer, Lipids, and Metabolism
- Endoplasmic Reticulum Stress and Disease
- Genetic factors in colorectal cancer
- CRISPR and Genetic Engineering
- Trace Elements in Health
- Science, Research, and Medicine
- Dietary Effects on Health
- Glycosylation and Glycoproteins Research
- Biomedical Research and Pathophysiology
- Mesenchymal stem cell research
- Ubiquitin and proteasome pathways
- Digestive system and related health
- Genetics and Neurodevelopmental Disorders
- DNA Repair Mechanisms
- Protein Degradation and Inhibitors
- Drug Transport and Resistance Mechanisms
The University of Texas MD Anderson Cancer Center
2017-2025
Sun Yat-sen University
2019
Sun Yat-sen Memorial Hospital
2019
Peking University
2014-2019
Targeting ferroptosis, a unique cell death modality triggered by unrestricted lipid peroxidation, in cancer therapy is hindered our incomplete understanding of ferroptosis mechanisms under specific genetic contexts. KEAP1 (kelch-like ECH associated protein 1) frequently mutated or inactivated lung cancers, and mutant cancers are refractory to most therapies, including radiotherapy. In this study, we identify suppressor 1 (FSP1, also known as AIFM2) transcriptional target nuclear factor...
The cystine transporter solute carrier family 7 member 11 (SLC7A11; also called xCT) protects cancer cells from oxidative stress and is overexpressed in many cancers. Here we report a surprising finding that, whereas moderate overexpression of SLC7A11 beneficial for treated with H2O2, common inducer, its high dramatically increases H2O2-induced cell death. Mechanistically, uptake combination H2O2 treatment results toxic buildup intracellular other disulfide molecules, NADPH depletion, redox...
The molecular mechanism controlling the zygotic genome activation (ZGA) in mammals remains poorly understood. 2-cell (2C)-like cells spontaneously emerging from cultures of mouse embryonic stem (ESCs) share some key transcriptional and epigenetic programs with 2C-stage embryos. By studying transition ESCs into 2C-like cells, we identified developmental pluripotency associated 2 4 (Dppa2/4) as important regulators program through directly up-regulating expression double homeobox (Dux). In...
Abstract Resistance to poly (ADP-ribose) polymerase inhibitors (PARPi) limits the therapeutic efficacy of PARP inhibition in treating breast cancer susceptibility gene 1 (BRCA1)-deficient cancers. Here we reveal that BRCA1 has a dual role regulating ferroptosis. promotes transcription voltage-dependent anion channel 3 (VDAC3) and glutathione peroxidase 4 (GPX4); consequently, deficiency cellular resistance erastin-induced ferroptosis but sensitizes cells induced by GPX4 (GPX4i). In addition,...
Ferroptosis has been recognized as a unique cell death modality driven by excessive lipid peroxidation and unbalanced cellular metabolism. In this study, we established protein interaction landscape for ferroptosis pathways through proteomic analyses, identified choline/ethanolamine phosphotransferase 1 (CEPT1) lysophosphatidylcholine acyltransferase 3 (LPCAT3)-interacting that regulates LPCAT3 stability. contrast to its known role in promoting phospholipid synthesis, showed CEPT1 suppresses...
Abstract Cellular sensitivity to ferroptosis is primarily regulated by mechanisms mediating lipid hydroperoxide detoxification. We show that inositol-requiring enzyme 1 (IRE1α), an endoplasmic reticulum (ER) resident protein critical for the unfolded response (UPR), also determines cellular ferroptosis. Cancer and normal cells depleted of IRE1α gain resistance ferroptosis, while enhanced expression promotes Mechanistically, IRE1α’s endoribonuclease activity cleaves down-regulates mRNA key...
The embryonic stem cell (ESC)-enriched miR-294/302 family and the somatic cell-enriched let-7 stabilizes self-renewing differentiated fates, respectively. mechanisms underlying these processes remain unknown. Here we show that among many pathways regulated by miR-294/302, combinatorial suppression of epithelial–mesenchymal transition (EMT) apoptotic is sufficient in maintaining self-renewal ESCs. silencing ESC was accompanied upregulation several EMT regulators induction apoptosis. ectopic...
The lack of a reliable and specific marker for ferroptosis has hindered the advancement treatments related to this cell death mechanism toward clinical application. A recent study published in
<div>Abstract<p>Resistance to poly (ADP-ribose) polymerase inhibitors (PARPi) limits the therapeutic efficacy of PARP inhibition in treating breast cancer susceptibility gene 1 (<i>BRCA1</i>)-deficient cancers. Here we reveal that BRCA1 has a dual role regulating ferroptosis. promotes transcription voltage-dependent anion channel 3 (<i>VDAC3</i>) and glutathione peroxidase 4 (<i>GPX4</i>); consequently, <i>BRCA1</i> deficiency...
<p>Supplementary Figure S1 shows that BRCA1 deficiency promotes GPX4i–induced ferroptosis. Supplementary S2 regulates GPX4 through the BRCT domain. S3 suppresses erastin-induced ferroptosis via interference with VDAC3 transcription and mitochondrial lipid peroxidation.Supplementary S4 PARPi synergize GPX4i in BRCA1-deficient cancers S5 combined BRCA1-mutant/deficient or homologous-recombination-restored cells tumors. S6 NCOA4-mediated ferritinophagy coupled defective induction...
<div>Abstract<p>Resistance to poly (ADP-ribose) polymerase inhibitors (PARPi) limits the therapeutic efficacy of PARP inhibition in treating breast cancer susceptibility gene 1 (<i>BRCA1</i>)-deficient cancers. Here we reveal that BRCA1 has a dual role regulating ferroptosis. promotes transcription voltage-dependent anion channel 3 (<i>VDAC3</i>) and glutathione peroxidase 4 (<i>GPX4</i>); consequently, <i>BRCA1</i> deficiency...
<p>Supplementary Figure S1 shows that BRCA1 deficiency promotes GPX4i–induced ferroptosis. Supplementary S2 regulates GPX4 through the BRCT domain. S3 suppresses erastin-induced ferroptosis via interference with VDAC3 transcription and mitochondrial lipid peroxidation.Supplementary S4 PARPi synergize GPX4i in BRCA1-deficient cancers S5 combined BRCA1-mutant/deficient or homologous-recombination-restored cells tumors. S6 NCOA4-mediated ferritinophagy coupled defective induction...