HIF1α regulated expression of XPA contributes to cisplatin resistance in lung cancer
Open accessAbstract
Factors regulating nucleotide excision repair probably contribute to the heterogenous response of advanced stage lung cancer patients to drugs such as cisplatin. Studies to identify the genes in the nucleotide excision repair pathway most closely associated with resistance to cisplatin have not been conclusive. We hypothesized that Xeroderma pigmentosum complementation group A (XPA), because of its dual role in sensing and recruiting other DNA repair proteins to the damaged template, would be critical in defining sensitivity to cisplatin. Studies were conducted to identify factors regulating transcription of XPA, to assess its role in modulating sensitivity to cisplatin and its expression in primary lung tumors. Hypoxia-inducible factor 1 alpha (HIF1α) subunit was found to bind with strong affinity to a hypoxia response element sequence in the promoter of XPA. Modulating expression of HIF1α by small interfering RNA or cobalt chloride markedly reduced or increased transcription of XPA in lung cancer cell lines, respectively. Protein levels of XPA were strongly correlated with sensitivity to cisplatin (r = 0.88; P < 0.001) in cell lines and sensitivity could be increased by small interfering RNA depletion of XPA. Expression of XPA determined in 54 primary lung tumors was elevated on average 5.2-fold when compared with normal bronchial epithelial cells and correlated with levels of HIF1α (r = 0.58; P < 0.01). Together, these studies identify XPA as a novel target for regulation by HIF1α whose modulation could impact lung cancer therapy.
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XPA may serve as a potential target for sensitization to cancer chemotherapy (e.g. cisplatin) via manipulation of available nuclear XPA, either at the transcriptional or post-transcriptional level.
“XPA may serve as a potential target for sensitization to cancer chemotherapy (e.g. cisplatin) via manipulation of available nuclear XPA, either at the transcriptional or post-transcriptional level [53], [54], [55].”
From UV-Induced Nuclear Import of XPA Is Mediated by Importin-α4 in An ATR-Dependent Manner (2013) · cites this paper as [54]
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- Authors
- Liu, Y., Bernauer, A. M., Yingling, C. M., & Belinsky, S. A.
- Affiliations
- Lovelace Respiratory Research Institute (US)
- Corresponding author
- Belinsky, Steven A.
- Venue
- Carcinogenesis
- Publisher
- Oxford University Press (OUP)
- Published
- 2012-03-31
- Volume
- 33
- Issue
- 6
- Pages
- 1187-1192
- ISSN
- 0143-3334 (ISSN-L)
- 1460-2180
- PMC
- PMC3388491
- OpenAlex
- W2148990963
- Cited by
- 65
- References
- 44
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 1 · 2023: 1 · 2022: 3 · 2021: 4 · 2020: 7 · 2019: 6 · 2018: 4 · 2017: 8 · 2016: 5 · 2015: 4 · 2014: 4 · 2013: 8 · 2012: 2
- FWCI
- 2.31
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Carcinogenesis (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Environmental Health Sciences (R01ES015262)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Health Sciences › Medicine › Oncology › Metal complexes synthesis and properties
- Keywords
- XPA, HIF-1α, cisplatin resistance, lung cancer, nucleotide excision repair, hypoxia response element, transcriptional regulation, cobalt chloride, siRNA, primary lung tumor
- MeSH terms
- Adenocarcinoma of Lung, Adenocarcinoma, Antineoplastic Agents, Cisplatin, Cobalt, DNA Repair, DNA-Binding Proteins, Humans, Lung Neoplasms, Transcription, Genetic, Gene Expression Regulation, Neoplastic, Drug Resistance, Neoplasm, RNA Interference, RNA, Small Interfering, Cell Line, Tumor, Xeroderma Pigmentosum Group A Protein, Hypoxia-Inducible Factor 1, alpha Subunit
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