ArticleBMC cancer2020
Proteomics reveals a therapeutic vulnerability via the combined blockade of APE1 and autophagy in lung cancer A549 cells.
Article in BMC cancer, 2020. 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, 20 citations in OpenAlex.
- Autophagy initiation inhibition combined with chemotherapy reverses drug resistance in oral cancer.Discover oncology · 2026Review
- An overview of autophagy inhibition as a potential clinical strategy in cancer therapy.Molecular pharmacology · 2025Review
- Live-cell imaging of human apurinic/apyrimidinic endonuclease 1 in the nucleus and nucleolus using a chaperone@DNA probe.Nucleic acids research · 2024Article
- Insight into autophagy in platinum resistance of cancer.International journal of clinical oncology · 2023Review
- Is Autophagy Always a Barrier to Cisplatin Therapy?Biomolecules · 2022Review
- SOX2 knockdown with siRNA reverses cisplatin resistance in NSCLC by regulating APE1 signaling.Medical oncology (Northwood, London, England) · 2022Article
- Targeting DNAJC19 overcomes tumor growth and lung metastasis in NSCLC by regulating PI3K/AKT signaling.Cancer cell international · 2021Article
- Traditional Herbal Medicine: A Potential Therapeutic Approach for Adjuvant Treatment of Non-small Cell Lung Cancer in the Future.Integrative cancer therapiesReview
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundDrug resistance is a major cause of therapeutic failure that is often associated with elevated autophagy and apurinic/apyrimidinic endonuclease 1 (APE1) expression. Herein, we investigated the role of APE1 and autophagy in A549 cells treated with cisplatin.
methodsSILAC proteomics was applied to obtain a panoramic view of cisplatin treatment in KRAS
resultsSILAC proteomics revealed that 72 canonical pathways, including base excision repair (BER) and autophagy signalling pathways, were regulated after cisplatin treatment in A549 cells. Cisplatin markedly induced autophagy and apoptosis in A549 cells, accompanied by remarkable APE1 increase. Suppression of autophagy enhanced the inhibition effect of cisplatin on cell growth, proliferation, and colony formation; however, APE1 inhibition enhanced the expression of LC3-I/II, suggesting that APE1 and autophagy are compensatory for cell survival to evade the anticancer action of cisplatin. Immunoprecipitation results revealed the triple complex of APE1-p53-LC3 in response to cisplatin plus CQ in A549 cells. Dual inhibition of APE1 and autophagy significantly enhanced cisplatin-induced apoptosis, which eventually overcame drug resistance in cisplatin-resistant A549 cells.
conclusionsDual inhibition of APE1 and autophagy greatly enhances apoptosis in parental KRAS
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