ArticleInternational journal of molecular sciences2023
GNAQ-Regulated ZO-1 and ZO-2 Act as Tumor Suppressors by Modulating EMT Potential and Tumor-Repressive Microenvironment in Lung Cancer.
Article in International journal of molecular sciences, 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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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- RBM15 drives bladder cancer progression through YTHDF2-dependent m6A-mediated regulation of ZO2.Journal of experimental & clinical cancer research : CR · 2026Article
- Small RNA sequencing identifies tsRNA-05020 as a potential regulator of cervical cancer progression.Turkish journal of biology = Turk biyoloji dergisi · 2026Article
- Rotenone inhibited osteosarcoma metastasis by modulating ZO-2 expression and location via the ROS/CaRedox report : communications in free radical research · 2025Article
- Targeted long-read methylation analysis using hybridization capture suitable for clinical specimens.Cell reports methods · 2025Article
- Loss of Zonula Occludens-1 (ZO-1) Enhances Angiogenic Signaling in Ovarian Cancer Cells.International journal of molecular sciences · 2025Article
- [High expression of SURF4 promotes migration, invasion and proliferation of gastric cancer cells by inhibiting tight junction proteins].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- SJB2-043, a USP1 Inhibitor, Suppresses A549 Cell Proliferation, Migration, and EMT via Modulation of PI3K/AKT/mTOR, MAPK, and Wnt Signaling Pathways.Current issues in molecular biology · 2025Article
- Gut microbiota: key facilitator in metastasis of colorectal cancer.Frontiers in oncology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Epithelial-to-mesenchymal transition (EMT) plays a critical role in the development and progression of lung cancer by promoting its invasiveness and metastasis. Using integrative analyses of the public lung cancer database, we found that the expression levels of the tight junction proteins, zonula occluden (ZO)-1 and ZO-2, were lower in lung cancer tissues, including both lung adenocarcinoma and lung squamous cell carcinoma than in normal lung tissues analyzed using The Cancer Genome Atlas (TCGA). Although the ectopic expression or knockdown of ZO-1 and ZO-2 did not affect the growth of lung cancer cells, they significantly regulated cell migration and invasion. When M0 macrophages were co-cultured with ZO-1 or ZO-2 knockdown Calu-1 cells, M2-like polarization was efficiently induced. Conversely, co-culture of M0 THP-1 cells with A549 cells stably expressing ZO-1 or ZO-2 significantly reduced M2 differentiation. We also identified G protein subunit alpha q (GNAQ) as a potential ZO-1- and ZO-2-specific activator through analysis of correlated genes with the TCGA lung cancer database. Our results suggest that the GNAQ-ZO-1/2 axis may play a tumor-suppressive role in lung cancer development and progression and highlight ZO-1 and ZO-2 as key EMT- and tumor microenvironment-suppressive proteins. These findings provide new insights for the development of targeted therapies for lung cancer.
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Registered trials
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