ArticleBMC cancer2023
Phosphorylation of TGIF2 represents a therapeutic target that drives EMT and metastasis of lung adenocarcinoma.
Article in BMC cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Transcriptional repression by TGIF2 coordinates neurogenic priming and neural stem cell maintenance.Science advances · 2026Article
- Synthesis and Development of Novel Small-Molecule MEIS2 Inhibitors That Induce Cell Death in Breast Cancer Cells by Targeting the Homeobox Domain.Pharmaceuticals (Basel, Switzerland) · 2026Article
- FBF1 maintains stem cell-like properties in breast cancer via PI3K/AKT/SOX2 axis.Stem cell research & therapy · 2025Article
- A Novel Competing Endogenous RNA Network Reveals Potential Mechanisms and Biomarkers of Chemoresistance in Lung Adenocarcinoma.Journal of Cancer · 2025Article
- SPP1 represents a therapeutic target that promotes the progression of oesophageal squamous cell carcinoma by driving M2 macrophage infiltration.British journal of cancer · 2024Article
- TGIF2 is a potential biomarker for diagnosis and prognosis of glioma.Frontiers in immunology · 2024Article
- Comprehensive analysis reveals TSPEAR as a prognostic biomarker in colorectal cancer.Journal of Cancer · 2024Article
- Advances in post-translational modifications of proteins and cancer immunotherapy.Frontiers in immunology · 2023Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTGF-β-induced factor homeobox 2 (TGIF2) is a transcription regulator that is phosphorylated by EGFR/ERK signaling. However, the functions of phosphorylated (p)-TGIF2 in cancer are largely unknown. Here, we investigated the roles of p-TGIF2 in promoting epithelial-mesenchymal transition (EMT) and metastasis in lung adenocarcinoma (LUAD).
methodsIn vitro and in vivo experiments were conducted to investigate the role of TGIF2 in LUAD EMT and metastasis. Dual-luciferase reporter and ChIP assays were employed to observe the direct transcriptional regulation of E-cadherin by TGIF2 and HDAC1. Co-immunoprecipitation was performed to identify the interaction between TGIF2 and HDAC1.
resultsDownregulating the expression of TGIF2 inhibited LUAD cell migration, EMT and metastasis in vitro and in vivo. Phosphorylation of TGIF2 by EGFR/ERK signaling was required for TGIF2-promoted LUAD EMT and metastasis since phosphorylation-deficient TGIF2 mutant lost these functions. Phosphorylation of TGIF2 was necessary to recruit HDAC1 to the E-cadherin promoter sequence and subsequently suppress E-cadherin transcription. Meanwhile, inhibition of HDAC1 repressed the TGIF2 phosphorylation-induced migration and EMT of LUAD cells. In xenograft mouse models, both inhibition of ERK and HDAC1 could significantly inhibited TGIF2-enhanced metastasis. Furthermore, TGIF2-positive staining was significantly correlated with E-cadherin-negative staining in human lung cancer specimens.
conclusionsOur study reveals the novel function of p-TGIF2 in promoting EMT and metastasis in LUAD; p-TGIF2 could be a potential therapeutic target to inhibit LUAD metastasis.
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