ArticleCancer medicine2019
Knockdown of SP1/Syncytin1 axis inhibits the proliferation and metastasis through the AKT and ERK1/2 signaling pathways in non-small cell lung cancer.
Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Evolutionary co-option of endogenous retroviruses: syncytins as regulators of placental development and disease.Molecular biology reports · 2026Review
- Chalcones as multitarget modulators in non-small cell lung cancer: mechanistic insights and therapeutic perspectives.Archives of toxicology · 2026Review
- The double-positive cells in the tumor microenvironment.Journal of translational internal medicine · 2026Article
- Implications of Heterotypic Cell Fusion in Cancer.Advances in experimental medicine and biology · 2026Review
- Function ofOncology letters · 2025Review
- Molecular Dynamics of Trogocytosis and Other Contact-Dependent Cell Trafficking Mechanisms in Tumor Pathogenesis.Cancers · 2025Review
- The role and therapeutic value of NUSAP1 in human cancers.Journal of translational medicine · 2025Review
- How Much Do You Fuse? A Comparison of Cell Fusion Assays in a Breast Cancer Model.International journal of molecular sciences · 2024Article
- SP1-activated USP27X-AS1 promotes hepatocellular carcinoma progression via USP7-mediated AKT stabilisation.Clinical and translational medicine · 2024Article
- Cell Fusion and Syncytia Formation in Cancer.Results and problems in cell differentiation · 2024Review
- Molecular mechanisms of syncytin-1 in tumors and placental development related diseases.Discover oncology · 2023Review
- NUSAP1 Binds ILF2 to Modulate R-Loop Accumulation and DNA Damage in Prostate Cancer.International journal of molecular sciences · 2023Article
- Sp1 Plays a Key Role in Vasculogenic Mimicry of Human Prostate Cancer Cells.International journal of molecular sciences · 2022Article
- Transcriptional and reverse transcriptional regulation of host genes by human endogenous retroviruses in cancers.Frontiers in microbiology · 2022Review
- Prognostic Significance and Therapeutic Target of CXC Chemokines in the Microenvironment of Lung Adenocarcinoma.International journal of general medicine · 2022Article
- Advanced bioinformatic analysis and pathway prediction of NSCLC cells upon cisplatin resistance.Scientific reports · 2021Article
- An Ancestral Retrovirus Envelope Protein Regulates Persistent Gammaherpesvirus Lifecycles.Frontiers in microbiology · 2021Article
- Article
- Long Non-Coding RNA LINC00491 Contributes to the Malignancy of Non-Small-Cell Lung Cancer via Competitively Binding to microRNA-324-5p and Thereby Increasing Specificity Protein 1 Expression.Cancer management and research · 2020Article
- Knockdown of SP1/Syncytin1 axis inhibits the proliferation and metastasis through the AKT and ERK1/2 signaling pathways in non-small cell lung cancer.Cancer medicine · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Syncytin 1 is considered as an oncogene in various malignant tumors, but its effect on non-small cell lung cancer (NSCLC) has not been reported. We investigated the specific role of Syncytin 1 on NSCLC through the transfection of Syncytin 1 knockdown or overexpression plamids in A549 cells. Our results proved that knockdown of Syncytin 1 inhibited the proliferation, and blocked the cell cycle on G1 phase by inhibiting the expression of Nusap1, Cyclin D1, CDK6, and CDK4. Cell cycle arrest also leaded to increased apoptosis in Syncytin 1 knockdown cells. Suppression of Syncytin 1 inhibited the migration and invasion, as well as the expressions of epithelial-mesenchymal transition (EMT) makers, N-cadherin, β-catenin, and Vimentin, indicating that Syncytin 1 knockdown inhibited the metastasis via reversing the EMT process in A549 cells. The phosphorylation levels of Akt, mTOR, and Erk1/2 were all decreased in Syncytin 1 knockdown cells, suggesting the signaling pathways by which Syncytin 1 operated as an oncogene in NSCLC. Moreover, the underexpression of transcription factor SP1 downregulated the Syncytin 1 expression in A549 cells. The rescue experiment of Syncytin 1 in SP1 knockdown cells further proved that Syncytin 1 could block the inhibition of cell growth induced by SP1 knockdown. In conclusion, knockdown of SP1/Syncytin1 axis inhibited the progression of NSCLC by the reversion of tumor epithelial-mesenchymal transition process and suppression of Akt and Erk signaling pathways, suggesting that they are potential targets for targeted therapy of NSCLC.
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