ArticleEndocrine2025
Anillin interacts with RhoA to promote tumor progression in anaplastic thyroid cancer by activating the PI3K/AKT pathway.
Article in Endocrine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
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Who cites it
7 citing papers in PubMed.
- Tumor microenvironment-guided targeted and immunotherapy in anaplastic thyroid cancer: a literature review from preclinical models to clinical translation.Translational cancer research · 2026Review
- VIRMA/IGF2BP3-mediated ANLN upregulation promotes intrahepatic cholangiocarcinoma growth by forming a positive feedback loop with RhoA/YAP1/TEAD1 signaling pathway.Cell death & disease · 2026Article
- Clinical and genetic diagnosis of a patient with focal segmental glomerulosclerosis due to a novel variant of the ANLN gene.CEN case reports · 2026Article
- Artificial intelligence in endocrine practice: comparing ChatGPT, Gemini, and Claude for adrenal incidentaloma care.Journal of endocrinological investigation · 2026Article
- The role of ANLN in malignant tumors: pathogenesis, treatment resistance and targeted strategies.Frontiers in cell and developmental biology · 2025Review
- Identification of potential pathogenic genes for urolithiasis through multi-omics Mendelian randomization analysis.Urolithiasis · 2024Article
- Strong Association Between Higher Expression of Anillin Actin-binding Protein in Pancreatic Adenocarcinoma Tissues and Patient Survival Analyzed With the UALCAN and GEPIA Platforms Using the TCGA Database.Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundAnaplastic thyroid cancer (ATC) is the most aggressive thyroid malignancy and has an extremely poor prognosis, necessitating novel therapeutic strategies. This study investigated the role of anillin (ANLN) in ATC, focusing on its impact on tumor growth and metastasis through the RhoA/PI3K/AKT signaling pathway.
methodsTCGA and GEO datasets were analyzed to identify key molecular alterations in thyroid cancer. ANLN expression was assessed in clinical samples. Functional assays, including CCK-8, colony formation, scratch, and Transwell invasion assays, and mouse xenograft models, were conducted to evaluate the biological role of ANLN. Coimmunoprecipitation, immunofluorescence, and active Rho GTPase pull-down assays, as well as phosphorylation antibody arrays, were used to explore the underlying mechanisms.
resultsAnalysis of TCGA and GEO datasets revealed that ANLN is upregulated in thyroid cancers, including ATC and PTC, with higher ANLN expression correlating with worse survival outcomes. Functional studies demonstrated that ANLN promoted ATC cell proliferation, migration, and invasion. In vivo, ANLN knockdown inhibited tumor growth in xenograft models. Mechanistically, ANLN directly interacted with RhoA, facilitating its activation and subsequent stimulation of the PI3K/AKT signaling pathway. The tumorigenic effects of ANLN were suppressed by AKT inhibition with afuresertib or RhoA silencing.
conclusionANLN plays a crucial role in ATC progression by activating the RhoA/PI3K/AKT pathway, suggesting its potential as a therapeutic target in ATC.
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Registered trials
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