ArticleOncology reports2020
Mitochondrial APE1 promotes cisplatin resistance by downregulating ROS in osteosarcoma.
Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- AK3 as a Hypoxia-Angiogenesis-Related Prognostic Biomarker and Therapeutic Target in Clear Cell Renal Cell Carcinoma.International journal of general medicine · 2026Article
- The role of cisplatin in modulating the tumor immune microenvironment and its combination therapy strategies: a new approach to enhance anti-tumor efficacy.Annals of medicine · 2025Review
- APE1 promotes lung adenocarcinoma through G4-mediated transcriptional reprogramming of urea cycle metabolism.iScience · 2025Article
- High APEX1 Expression Facilitates Osteosarcoma Cell Proliferation.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Targeting APE1: Advancements in the Diagnosis and Treatment of Tumors.Protein and peptide letters · 2025Review
- APE1 mediates chemoresistance in esophageal squamous cell carcinoma by remodeling the immunosuppressive microenvironment.Frontiers in immunology · 2025Article
- Isoliensinine exerts antitumor effects in lung adenocarcinoma by inhibiting APEX1-driven ROS production.Frontiers in pharmacology · 2025Article
- Targeting the mitochondrial protein YME1L to inhibit osteosarcoma cell growth in vitro and in vivo.Cell death & disease · 2024Article
- Apurinic/apyrimidinic endodeoxyribonuclease 1 (APE1) promotes stress granule formation via YBX1 phosphorylation in ovarian cancer.Cellular and molecular life sciences : CMLS · 2024Article
- Targeting POLRMT by a first-in-class inhibitor IMT1 inhibits osteosarcoma cell growth in vitro and in vivo.Cell death & disease · 2024Article
- The APE1/REF-1 and the hallmarks of cancer.Molecular biology reports · 2024Review
- Revisiting Two Decades of Research Focused on Targeting APE1 for Cancer Therapy: The Pros and Cons.Cells · 2023Review
- ROS-Induced Mitochondrial Dysfunction in CD4 T Cells from ART-Controlled People Living with HIV.Viruses · 2023Article
- ADCK1 is a potential therapeutic target of osteosarcoma.Cell death & disease · 2022Article
- APE1 shRNA-loaded cancer stem cell-derived extracellular vesicles reverse Erlotinib resistance in non-small cell lung cancer via the IL-6/STAT3 signalling.Clinical and translational medicine · 2022Article
- Epithelial to Mesenchymal Transition Relevant Subtypes with Distinct Prognosis and Responses to Chemo- or Immunotherapies in Osteosarcoma.Journal of immunology research · 2022Article
- Effects of osteoblast-derived extracellular vesicles on aggressiveness, redox status and mitochondrial bioenergetics of MNNG/HOS osteosarcoma cells.Frontiers in oncology · 2022Article
- Potential Role of APEX1 During Ferroptosis.Frontiers in oncology · 2022Review
- Elucidating Role of Reactive Oxygen Species (ROS) in Cisplatin Chemotherapy: A Focus on Molecular Pathways and Possible Therapeutic Strategies.Molecules (Basel, Switzerland) · 2021Review
- Targeting TFE3 Protects Against Lysosomal Malfunction-Induced Pyroptosis in Random Skin Flaps via ROS Elimination.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apurinic/apyrimidinic endonuclease 1 (APE1) is a primary nuclear‑localized multifunctional protein in osteosarcoma. However, the cytoplasmic localization of APE1 was found to be functional and to increase with cisplatin resistance, yet the molecular mechanism is unknown. In the present study, we explored the cisplatin resistance mechanism in osteosarcoma from the new perspective of APE1 extranuclear biological activity. Using cisplatin‑resistant and cisplatin‑sensitive osteosarcoma cell lines, we found that mitochondrial APE1 (mtAPE1) was overexpressed in cisplatin‑resistant cells but not in sensitive cells. Overexpression of mtAPE1 reduced cisplatin‑induced apoptosis, while knockdown of APE1 reversed this phenomenon and caused oxidative DNA damage via overproduction of reactive oxygen species (ROS). We further demonstrated that high mtAPE1 expression could downregulate ROS production by decreasing the phosphorylation of Rac1 (p‑Rac1), further promoting cisplatin resistance in osteosarcoma. Our findings suggest that mitochondrial APE1 promotes cisplatin resistance by decreasing ROS generation, which may provide new ideas for researching the molecular mechanism of osteosarcoma chemoresistance and strategies to overcome cisplatin resistance in osteosarcoma.
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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.