ArticleWorld journal of clinical oncology2024
Tankyrase 2 promotes lung cancer cell malignancy.
Article in World journal of clinical oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Isatin-based oxime ethers as anticancer agents against human colorectal carcinoma.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Tankyrases and Their Binding Proteins: Origins of Their Roles in Diverse Cellular Pathways.Cells · 2026Review
- Roles of ADP-Ribosyltransferases in Cancer.Oncology research · 2026Review
- Apoptosis and G2/M Phase Cell Cycle Arrest Induced by Alkaloid Erythraline Isolated fromInternational journal of molecular sciences · 2025Article
- Tankyrase 2 as a therapeutic target in non-small cell lung cancer: Implications for apoptosis and migration.World journal of clinical oncology · 2025Article
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTankyrase 2 (TNKS2) is a potential candidate molecular target for the prognosis and treatment of non-small cell lung cancer (NSCLC), but its biological functions are unclear.
aimTo investigate the biological functions of TNKS2 in NSCLC.
methodsUsing a lentiviral vector, we generated H647 model cells with TNKS2 knockdown by RNA interference and A549 model cells with TNKS2 overexpression by transfection with a TNKS2 overexpressing plasmid. Increased and decreased expression levels of TNKS2 in the two cell lines were verified using real-time reverse transcriptase-polymerase chain reaction and Western blot analyses. Cell apoptosis, proliferation, and migration were determined using flow cytometry, carboxyfluorescein succinimidyl ester staining, and scratch assay, respectively. Immunofluorescence staining was conducted to examine TNKS2 and β-catenin expression levels in the two transfected cell lines and the non-transfected cells.
resultsTNKS2 mRNA and protein expression was significantly higher in the highly malignant NCI-H647 cells, while it remained at a low level in the less malignant A549 cells. Lentivirus-mediated overexpression of TNKS2 in A549 cells resulted in a 3-fold increase in gene expression and a 1.7-fold increase in protein expression (
conclusionThe obtained results revealed that TNKS2 may serve as an adverse prognostic factor and a potential therapeutic target in NSCLC.
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