ArticleOncology letters2018
Survivin expression modulates the sensitivity of A549 lung cancer cells resistance to vincristine.
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 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- Targeting the inhibitors of apoptosis proteins (IAPs) to combat drug resistance in cancers.Frontiers in pharmacology · 2025Review
- Vincristine in Cancer Therapy: Mechanisms, Efficacy, and Future Perspectives.Current medicinal chemistry · 2025Review
- Survivin in lung cancer: a potential target for therapy and prevention-a narrative review.Translational lung cancer research · 2024Review
- Article
- Antitumor Effect of Epigallocatechin Gallate and Vincristine in Mice with L5178Y Lymphoma.Plants (Basel, Switzerland) · 2023Article
- Suppression of Chromosome Instability Limits Acquired Drug Resistance.Molecular cancer therapeutics · 2022Article
- Selective Disruption of Survivin's Protein-Protein Interactions: A Supramolecular Approach Based on Guanidiniocarbonylpyrrole.Chembiochem : a European journal of chemical biology · 2022Article
- Network Pharmacology Integrated Molecular Docking to Explore the Mechanism of Blister Beetle Therapy for Lung Adenocarcinoma.Contrast media & molecular imaging · 2022Article
- Article
- Identification and validation of an autophagy-related long non-coding RNA signature as a prognostic biomarker for patients with lung adenocarcinoma.Journal of thoracic disease · 2021Article
- miR-421 promotes the viability of A549 lung cancer cells by targeting forkhead box O1.Oncology letters · 2020Article
- Synthesis, In Silico Prediction and In Vitro Evaluation of Antitumor Activities of Novel Pyrido[2,3-Molecules (Basel, Switzerland) · 2020Article
- Long Non-coding RNA LINC00628 Interacts Epigenetically with the LAMA3 Promoter and Contributes to Lung Adenocarcinoma.Molecular therapy. Nucleic acids · 2019Article
- Prognostic Value of BIRC5 in Lung Adenocarcinoma Lacking EGFR, KRAS, and ALK Mutations by Integrated Bioinformatics Analysis.Disease markers · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer is the leading cause of cancer-associated mortalities worldwide. Chemotherapeutic drug vincristine is widely used to treat lung cancer; however, the acquisition of drug resistance is the major limitation of chemotherapy, and it is thus important to determine the mechanism underlying vincristine resistance in lung cancer. Survivin has been reported to be associated with the development of drug resistance and be involved in the progression of non-small cell lung cancer. In the present study, a vincristine-resistant lung cancer cell line, A549/VCR, was used to investigate the possible involvement of survivin in the acquisition of vincristine resistance. Western blot analysis demonstrated that survivin protein expression level was markedly higher in A549/VCR cells compared with in control A549 cells, whereas p53 expression level was lower in A549/VCR cells compared with in A549 cells. Thus, wild-type p53 was overexpressed in A549/VCR cells and it reversed vincristine resistance of A549/VCR cells via the inhibition of survivin expression. Furthermore, survivin was knocked down by small interfering RNA technology and the effects on viability and apoptosis of resistant cells were investigated. MTT, Annexin V-fluorescein isothiocyanate/propidium iodide and caspase-3 activity assays indicated that survivin silencing significantly inhibited cell viability and enhanced apoptosis induced by vincristine treatment in A549/VCR cells compared with non-silenced A549/VCR cells. These results suggested that survivin expression regulated by p53 may serve an important role in drug resistance in A549/VCR cells and may be a potential target for enhancing vincristine sensitivity in A549 lung cancer cells. Additionally, the present study revealed that A549/VCR cells exhibited cross resistance to methotrexate (MTX) and survivin silencing re-sensitized A549/VCR cells to MTX, indicating the crucial role of survivin in regulating A549 cells sensitivity to anticancer drugs. The results of the present study are significant for determining the underlying mechanism of vincristine resistance in lung cancer.
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