ArticleCell cycle (Georgetown, Tex.)2016
Efficacy of poly (ADP-ribose) polymerase inhibitor olaparib against head and neck cancer cells: Predictions of drug sensitivity based on PAR-p53-NF-κB interactions.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- PARP Inhibitor Inhibits the Vasculogenic Mimicry through a NF-κB-PTX3 Axis Signaling in Breast Cancer Cells.International journal of molecular sciences · 2022Article
- Identification of PARP-1 in cancer stem cells of gastrointestinal cancers: A preliminary study.Journal of biosciences · 2021Article
- P53 vs NF-κB: the role of nuclear factor-kappa B in the regulation of p53 activity and vice versa.Cellular and molecular life sciences : CMLS · 2020Review
- ADP-Ribosylation Levels and Patterns Correlate with Gene Expression and Clinical Outcomes in Ovarian Cancers.Molecular cancer therapeutics · 2020Article
- Combining PARP and DNA-PK Inhibitors With Irradiation Inhibits HPV-Negative Head and Neck Cancer Squamous Carcinoma Growth.Frontiers in genetics · 2020Article
- Review
- Roles of DNA repair enzyme OGG1 in innate immunity and its significance for lung cancer.Pharmacology & therapeutics · 2019Review
- Identification of natural compounds targeting Annexin A2 with an anti-cancer effect.Protein & cell · 2018Article
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Authors and funding
4 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Poly (ADP-ribose) polymerase (PARP) is a key molecule in the DNA damage response (DDR), which is a major target of both chemotherapies and radiotherapies. PARP inhibitors therefore comprise a promising class of anticancer therapeutics. In this study, we evaluated the efficacy of the PARP inhibitor olaparib, and also sought to identify the mechanism and predictive marker associated with olaparib sensitivity in head and neck cancer (HNC) cells. A total of 15 HNC cell lines, including AMC HNC cells, were tested. AMC-HN3 and HN4 exhibited stronger responses to olaparib. Among cisplatin-resistant cell lines, only AMC HN9-cisR cells were significantly suppressed by olaparib. We found that basal poly (ADP-ribose) (PAR) levels, but not PARP-1 levels, correlated with olaparib sensitivity. AMC-HN3 and HN4 cells exhibited higher basal levels of NF-κB that decreased significantly after olaparib treatment. In contrast, apoptotic proteins were intrinsically expressed in AMC-HN9-cisR cells. As interference with p53 expression led to NF-κB reactivation, we concluded that elevated basal PAR and NF-κB levels are predictive of olaparib responsiveness in HNC cells; in addition, olaparib inhibits HNC cells via PAR-p53-NF-κB interactions.
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