ArticleJournal of cellular and molecular medicine2022
Vestigial-like family member 3 stimulates cell motility by inducing high-mobility group AT-hook 2 expression in cancer cells.
Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
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- The Molecular and Functional Landscape of Resistance to FOLFIRI Chemotherapy in Metastatic Colorectal Cancer.Cancer discovery · 2026Article
- Clinical risk prediction in lung adenocarcinoma using MAL gene and tumor microenvironment features.Discover oncology · 2026Article
- Roles of TEAD Transcription Factors and their Coactivators in the Progression and Metastasis of Cancers.Recent patents on anti-cancer drug discovery · 2026Review
- A complex mechanism translating variation of a simple genetic architecture into alternative life histories.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- VGLL3 modulates chemosensitivity through promoting DNA double-strand break repair.Science advances · 2024Article
- Article
- Vestigial-like family member 3 stimulates cell motility by inducing high-mobility group AT-hook 2 expression in cancer cells.Journal of cellular and molecular medicine · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Vestigial-like family member 3 (VGLL3) is a cofactor for TEA domain transcription factors (TEADs). Although VGLL3 is known to be highly expressed and stimulate cell proliferation in mesenchymal cancer cells, its involvement in mesenchymal phenotypes is largely unknown. In this study, we found that VGLL3 promotes epithelial-to-mesenchymal transition (EMT)-like phenotypic changes. We found that A549 human lung cancer cells stably expressing VGLL3 exhibit spindle-like morphological changes, reduction in the epithelial marker E-cadherin and induction of the mesenchymal marker Snail. Notably, VGLL3-expressing cells exhibited enhanced motility. The DNA-binding protein high-mobility group AT-hook 2 (HMGA2) was found to be a target of the VGLL3-TEAD4 complex, and HMGA2 knockdown repressed EMT-like phenotypic changes in VGLL3-expressing cells. VGLL3-dependent phenotypic changes are involved in transforming growth factor-β (TGF-β)-induced EMT progression. VGLL3 or HMGA2 knockdown repressed the motility of the mesenchymal breast cancer MDA-MB-231 cells. Importantly, high levels of VGLL3 expression were shown to have a positive correlation with poor prognosis in various human cancers, such as breast, colon, ovarian, head and neck, pancreatic, renal, gastric and cervical cancers. These results suggest that VGLL3 promotes EMT-like cell motility by inducing HMGA2 expression and accelerates cancer progression.
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