ArticleTranslational cancer research2020
Wnt7a inhibits transformed cell proliferation while promoting migration and invasion in non-small cell lung cancer.
Article in Translational cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Long-term high fat diet aggravates the risk of lung fibrosis and lung cancer: transcriptomic analysis in the lung tissues of obese mice.Translational lung cancer research · 2024Article
- WNT7A promotes tumorigenesis of head and neck squamous cell carcinoma via activating FZD7/JAK1/STAT3 signaling.International journal of oral science · 2024Article
- WNT ligands in non-small cell lung cancer: from pathogenesis to clinical practice.Discover oncology · 2023Review
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNon-small cell lung cancer (NSCLC) is the most important cause of lung cancer death. Wnt7a is a known tumor suppressor gene which is often downregulated in NSCLC, and restoration of Wnt7a leads to decreased NSCLC cell proliferation. However, the biological role of Wnt7a in the migration and invasion in NSCLC remains unclear.
methodsWe examined whether overexpression of Wnt7a transfected by pcDNA6-Wnt7a could induce the proliferation, migration and invasion of NSCLC H1650 and A549 cell lines. Wnt7a signaling pathway, such as canonical (β-catenin) or non-canonical (c-Jun N-terminal kinase, JNK) pathways, were also assessed.
resultsWe found that re-expression of Wnt7a led to reduced cell growth in NSCLC cell lines. In spite of the antiproliferative effect, Wnt7a overexpression could affect the migration and invasion of NSCLC cells. In the Wnt7a signaling pathway, the phosphorylation of JNK (Thr-183/Tyr-185) and c-Jun (Ser-63) were increased by re-expression of Wnt7a in both H1650 and A549 cell lines. The phosphorylation of β-catenin (Thr-41/Ser-45, Ser-552, Ser-675, and Ser-45) were not altered by restoration of Wnt7a. In NSCLC cells, Wnt7a overexpression was accompanied by parallel changes in the JNK pathway but not in the β-catenin pathway.
conclusionsThese results help to understand that Wnt7a may play a two-sided role in NSCLC, suggesting that restoration of Wnt7a expression is not always suitable as therapeutic strategy for NSCLC.
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