ArticleOncotarget2015
ZNF32 protects against oxidative stress-induced apoptosis by modulating C1QBP transcription.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- Identification of the oxidation stress-related gene signatures and functional verification of MINK1 in prostate cancer cells.PloS one · 2026Article
- Cyclophilin D reduces Ca2+ sequestration by complement 1q binding protein.The Biochemical journal · 2025Article
- Pan-cancer analysis and experimental validation revealed the prognostic role of ZNF83 in renal and lung cancer cohorts.Discover oncology · 2025Article
- Increased ZNF83 is a potential prognostic biomarker and regulates oxidative stress-induced ferroptosis in clear cell renal cell carcinoma.Journal of molecular medicine (Berlin, Germany) · 2025Article
- A pan-cancer analysis: predictive role of ZNF32 in cancer prognosis and immunotherapy response.Discover oncology · 2025Article
- ZNF32 histidine 179 and 183 single-site and double-site mutations promote nuclear speckle formation but differentially regulate the proliferation of breast cancer cells.Frontiers in cell and developmental biology · 2025Article
- Zinc finger proteins facilitate adaptation of a global insect pest to climate change.BMC biology · 2024Article
- Transcriptomic response of overexpression ZNF32 in breast cancer cells.Scientific reports · 2024Article
- Article
- An approach to p32/gC1qR/HABP1: a multifunctional protein with an essential role in cancer.Journal of cancer research and clinical oncology · 2022Review
- Prognostic and functional role of hyaluronan-binding protein 1 in pancreatic ductal adenocarcinoma.Oncology letters · 2022Article
- C1QBP regulates apoptosis of renal cell carcinoma via modulating xanthine dehydrogenase (XDH) mediated ROS generation.International journal of medical sciences · 2022Article
- Hsa‑circRNA‑G004213 promotes cisplatin sensitivity by regulating miR‑513b‑5p/PRPF39 in liver cancer.Molecular medicine reports · 2021Article
- NAMPT promotes hepatitis B virus replication and liver cancer cell proliferation through the regulation of aerobic glycolysis.Oncology letters · 2021Article
- Genome-Wide Association Study and Pathway Analysis for Heterophil/Lymphocyte (H/L) Ratio in Chicken.Genes · 2020Article
- Construction of a 14-lncRNA risk score system predicting survival of children with acute myelocytic leukemia.Experimental and therapeutic medicine · 2020Article
- High expression of ZNF93 promotes proliferation and migration of ovarian cancer cells and relates to poor prognosis.International journal of clinical and experimental pathology · 2020Article
- Complement component 1q subcomponent binding protein in the brain of the rat.Scientific reports · 2019Article
- The Tumor Suppressor Role of Zinc Finger Protein 671 (Frontiers in oncology · 2019Article
- Zinc finger protein 32 promotes breast cancer stem cell-like properties through directly promoting GPER transcription.Cell death & disease · 2018Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS)-driven oxidative stress has been recognized as a critical inducer of cancer cell death in response to therapeutic agents. Our previous studies have demonstrated that zinc finger protein (ZNF)32 is key to cell survival upon oxidant stimulation. However, the mechanisms by which ZNF32 mediates cell death remain unclear. Here, we show that at moderate levels of ROS, Sp1 directly binds to two GC boxes within the ZNF32 promoter to activate ZNF32 transcription. Alternatively, at cytotoxic ROS concentrations, ZNF32 expression is repressed due to decreased binding activity of Sp1. ZNF32 overexpression maintains mitochondrial membrane potential and enhances the antioxidant capacity of cells to detoxify ROS, and these effects promote cell survival upon pro-oxidant agent treatment. Alternatively, ZNF32-deficient cells are more sensitive and vulnerable to oxidative stress-induced cell injury. Mechanistically, we demonstrate that complement 1q-binding protein (C1QBP) is a direct target gene of ZNF32 that inactivates the p38 MAPK pathway, thereby exerting the protective effects of ZNF32 on oxidative stress-induced apoptosis. Taken together, our findings indicate a novel mechanism by which the Sp1-ZNF32-C1QBP axis protects against oxidative stress and implicate a promising strategy that ZNF32 inhibition combined with pro-oxidant anticancer agents for hepatocellular carcinoma treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.