ArticleOncology letters2018
Hypoxia exposure induced cisplatin resistance partially via activating p53 and hypoxia inducible factor-1α in non-small cell lung cancer A549 cells.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 28 citations in OpenAlex.
- Loss of the USP22 deubiquitylase confers resistance to chemotherapy in small cell lung cancer.Nature communications · 2026Article
- FOXO1 Inhibition and FADD Knockdown Have Opposing Effects on Anticancer Drug-Induced Cytotoxicity and p21 Expression in Osteosarcoma Cells.International journal of molecular sciences · 2026Article
- Review
- Hypoxia studies in non‑small cell lung cancer: Pathogenesis and clinical implications (Review).Oncology reports · 2025Review
- p21 promotes gemcitabine tolerance in A549 cells by inhibiting DNA damage and altering the cell cycle.Oncology letters · 2023Article
- Cytotoxicity of Ruthenium(II) Arene Complexes Containing Functionalized Ferrocenyl β-Diketonate Ligands.Organometallics · 2023Article
- Hypoxia and lactate influence VOC production in A549 lung cancer cells.Frontiers in molecular biosciences · 2023Article
- Current Landscape of Therapeutic Resistance in Lung Cancer and Promising Strategies to Overcome Resistance.Cancers · 2022Review
- Article
- FDA approved L-type channel blocker Nifedipine reduces cell death in hypoxic A549 cells through modulation of mitochondrial calcium and superoxide generation.Free radical biology & medicine · 2021Article
- Review
- Hypoxia increases the expression of stem cell markers in human osteosarcoma cells.Oncology letters · 2021Article
- Mechanisms of resistance to chemotherapy in non-small cell lung cancer.Archives of pharmacal research · 2021Review
- SIRT1/PGC-1α/PPAR-γ Correlate With Hypoxia-Induced Chemoresistance in Non-Small Cell Lung Cancer.Frontiers in oncology · 2021Review
- Interplay Between Thiamine and p53/p21 Axes Affects Antiproliferative Action of Cisplatin in Lung Adenocarcinoma Cells by Changing Metabolism of 2-Oxoglutarate/Glutamate.Frontiers in genetics · 2021Article
- The Mechanism of Warburg Effect-Induced Chemoresistance in Cancer.Frontiers in oncology · 2021Review
- Article
- Polymerized human hemoglobin increases the effectiveness of cisplatin-based chemotherapy in non-small cell lung cancer.Oncotarget · 2020Article
- [Role of P21 in Resistance of Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2020Review
- Activation of Mitochondrial 2-Oxoglutarate Dehydrogenase by Cocarboxylase in Human Lung Adenocarcinoma Cells A549 Is p53/p21-Dependent and Impairs Cellular Redox State, Mimicking the Cisplatin Action.International journal of molecular sciences · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer is one of the most frequently occurring and fatal cancer types worldwide. Cisplatin is widely used for chemotherapy of non-small cell lung cancer (NSCLC). However, the use of cisplatin has been met with the challenge of chemoresistance as a result of hypoxia, which is common in adult solid tumors and is a principal cause of a poor patient outcome. In the present study, the effects of hypoxia on the response of the NSCLC A549 cell line to the clinically relevant cytotoxic cisplatin were evaluated via regulating hypoxia inducible facor-1α (HIF-1α) and p53. Hypoxia exposure upregulated the expression levels of HIF-1α and p53, and promoted glycolysis in A549 cells, which was attenuated by HIF-1α knockdown by siRNA introduction, indicating the critical roles of HIF-1α in regulating glycolysis under hypoxic conditions. HIF-1α-knockdown also sensitized A549 cells to cisplatin in hypoxia-exposed, but not in normoxia-exposed A549 cells, suggesting that hypoxia-induced cisplatin resistance partially contributes toward the upregulation of HIF-1α by hypoxia exposure. The present study also determined that hypoxia-upregulated p53 activated its downstream target gene p21 transcriptionally and blocked the cell cycle at the G1-G0 phase, thereby leading to inhibition of cell proliferation. As a result, activated p53 desensitized A549 cells to cisplatin potentially through increasing the non-proliferation status of A549 cells and therefore minimizing the influence of cisplatin. Taken together, these results identified the exact effects of HIF-1α and p53 induced by hypoxia and potentially elucidated their protective effects on A549 cells against cisplatin.
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