ArticleOncotarget2016
Chronic TGFβ stimulation promotes the metastatic potential of lung cancer cells by Snail protein stabilization through integrin β3-Akt-GSK3β signaling.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Prognostic value of high-expression of miR-17-92 cluster in various tumors: evidence from a meta-analysis.Scientific reports · 2017Pooled it
- Deciphering the Role of ADAMTS6 in the Epithelial-Mesenchymal Transition of Lung Adenocarcinoma Cells.International journal of molecular sciences · 2025Article
- Concurrent targeting of GSK3 and MEK as a therapeutic strategy to treat pancreatic ductal adenocarcinoma.Cancer science · 2024Article
- Chronic Leptin Treatment Induces Epithelial-Mesenchymal Transition in MCF10A Mammary Epithelial Cells.Journal of mammary gland biology and neoplasia · 2022Article
- TGFβ promotes YAP-dependent AXL induction in mesenchymal-type lung cancer cells.Molecular oncology · 2021Article
- Systematic identification of a nuclear receptor-enriched predictive signature for erastin-induced ferroptosis.Redox biology · 2020Article
- Stochastic and Heterogeneous Cancer Cell Migration: Experiment and Theory.Scientific reports · 2019Article
- Crosstalk between cancer and immune cells: Role of tumor-associated macrophages in the tumor microenvironment.Cancer medicine · 2019Review
- Article
- LncRNA ANCR down-regulation promotes TGF-β-induced EMT and metastasis in breast cancer.Oncotarget · 2017Article
- Cytosolic THUMPD1 promotes breast cancer cells invasion and metastasis via the AKT-GSK3-Snail pathway.Oncotarget · 2017Article
- TGFΒ-induced transcription in cancer.Seminars in cancer biology · 2017Review
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8 authors.
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Abstract
Chronic exposure to TGFβ, a frequent occurrence for tumor cells in the tumor microenvironment, confers more aggressive phenotypes on cancer cells by promoting their invasion and migration while at the same time increasing their resistance to the growth-inhibitory effect of TGFβ. In this study, a transdifferentiated (TD) A549 cell model, established by chronically exposing A549 cells to TGFβ, showed highly invasive phenotypes in conjunction with attenuation of Smad-dependent signaling. We show that Snail protein, the mRNA expression of which strongly correlates with a poor prognosis in lung cancer patients, was highly stable in TD cells after TGFβ stimulation. The increased protein stability of Snail in TD cells correlated with elevated inhibitory phosphorylation of GSK3β, resulting from the high Akt activity. Notably, integrin β3, whose expression was markedly increased upon sustained exposure to TGFβ, was responsible for the high Akt activity as well as the increased Snail protein stability in TD cells. Consistently, clinical database analysis on lung cancer patients revealed a negative correlation between overall survival and integrin β3 mRNA levels. Therefore, we suggest that the integrin β3-Akt-GSK3β signaling axis plays an important role in non-canonical TGFβ signaling, determining the invasive properties of tumor cells chronically exposed to TGFβ.
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