ArticleOncogene2008
Combinatorial action of the HDAC inhibitor trichostatin A and etoposide induces caspase-mediated AIF-dependent apoptotic cell death in non-small cell lung carcinoma cells.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
31 citing papers in PubMed, 63 citations in OpenAlex.
- HDAC Inhibitors Enhance the Chemosensitivity of Osteosarcoma Cells to Etoposide by Suppressing the Hippo/YAP Signaling Pathway.International journal of molecular sciences · 2025Article
- Pharmacological Properties of Trichostatin A, Focusing on the Anticancer Potential: A Comprehensive Review.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Article
- Valeric Acid Suppresses Liver Cancer Development by Acting as a Novel HDAC Inhibitor.Molecular therapy oncolytics · 2020Article
- The Role of Histone Acetylation-/Methylation-Mediated Apoptotic Gene Regulation in Hepatocellular Carcinoma.International journal of molecular sciences · 2020Review
- Identification of molecular markers associated with the progression and prognosis of endometrial cancer: a bioinformatic study.Cancer cell international · 2020Article
- Inhibition of BET Proteins and Histone Deacetylase (HDACs): Crossing Roads in Cancer Therapy.Cancers · 2019Review
- Identification of Potential Biomarkers in Association With Progression and Prognosis in Epithelial Ovarian Cancer by Integrated Bioinformatics Analysis.Frontiers in genetics · 2019Article
- Identification of key candidate genes and small molecule drugs in cervical cancer by bioinformatics strategy.Cancer management and research · 2018Article
- Correlation between histone acetylation and expression of Notch1 in human lung carcinoma and its possible role in combined small-cell lung carcinoma.Laboratory investigation; a journal of technical methods and pathology · 2017Article
- Article
- Superior efficacy of co-treatment with the dual PI3K/mTOR inhibitor BEZ235 and histone deacetylase inhibitor Trichostatin A against NSCLC.Oncotarget · 2016Article
- Trichostatin A Enhances the Apoptotic Potential of Palladium Nanoparticles in Human Cervical Cancer Cells.International journal of molecular sciences · 2016Article
- Effects of histone deacetylase inhibitor trichostatin A combined with cisplatin on apoptosis of A549 cell line.Thoracic cancer · 2015Article
- Molecular mechanisms of etoposide.EXCLI journal · 2015Review
- Heat-modified citrus pectin induces apoptosis-like cell death and autophagy in HepG2 and A549 cancer cells.PloS one · 2015Article
- Epigenetics and miRNA as predictive markers and targets for lung cancer chemotherapy.Cancer biology & therapy · 2015Article
- Inhibitors of histone deacetylases enhance neurotoxicity of DNA damage.Neuromolecular medicine · 2014Article
- Integrative genomics: quantifying significance of phenotype-genotype relationships from multiple sources of high-throughput data.Frontiers in genetics · 2012Article
- Functional characterization of CLPTM1L as a lung cancer risk candidate gene in the 5p15.33 locus.PloS one · 2012Article
Corrections and comments
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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
Commonly used regimens in cancer therapy rely on the induction of apoptotic cell death, and drug resistance can be attributed, at least in part, to a disabled apoptotic program. Non-small cell lung carcinomas (NSCLC), exhibit an intrinsic resistance to chemotherapy. Here, we show that co-treatment with etoposide (VP16) and the pan-histone deacetylase (HDAC) inhibitor trichostatin A (TSA), but not valproic acid (VPA), induced apoptotic cell death in drug-resistant NSCLC cells. Co-treatment, but not single treatment, with VP16 and TSA induced apoptosis in a caspase-dependent manner accompanied by a crucial decrease in Bcl-xL expression allowing Bax activation and subsequent initiation of the apoptosis inducing factor (AIF)-dependent death pathway. Importantly, AIF proved to be required for the effects of TSA/VP16 as RNA knockdown of AIF resulted in a complete abolishment of TSA/VP16-induced apoptotic cell death in drug-resistant NSCLC cells. Our results thus provide evidence for the requirement of both caspase-dependent and caspase-independent apoptotic pathways in TSA/VP16-mediated death of drug-resistant NSCLC cells, and extend previous suggestions that HDAC inhibitors in combination with conventional chemotherapeutic drugs could be valuable in the treatment of NSCLC cancer and other malignancies in which Bcl-xL is overexpressed.
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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.