Related Experiment Video
Updated: Jun 4, 2025

Spontaneous Murine Model of Anaplastic Thyroid Cancer
Published on: February 3, 2023
Anillin interacts with RhoA to promote tumor progression in anaplastic thyroid cancer by activating the PI3K/AKT
Shi-Tong Yu1, Bai-Hui Sun1, Jun-Na Ge1
1Department of General Surgery, Nanfang Hospital, The First School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong Province, China.
Background:
Anaplastic 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.
Methods:
TCGA 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.
Results:
Analysis 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.
Conclusion:
ANLN plays a crucial role in ATC progression by activating the RhoA/PI3K/AKT pathway, suggesting its potential as a therapeutic target in ATC.
Insights
Anillin (ANLN) drives anaplastic thyroid cancer (ATC) growth and spread by activating the RhoA/PI3K/AKT pathway. Targeting ANLN may offer a new therapeutic strategy for this aggressive cancer.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Anaplastic thyroid cancer (ATC) is highly aggressive with a poor prognosis.
- Novel therapeutic strategies are urgently needed for ATC.
- This study explores the role of anillin (ANLN) in ATC progression.
Purpose of the Study:
- Investigate the role of anillin (ANLN) in anaplastic thyroid cancer (ATC).
- Determine the impact of ANLN on tumor growth and metastasis.
- Elucidate the involvement of the RhoA/PI3K/AKT signaling pathway.
Main Methods:
- Analysis of TCGA and GEO datasets for molecular alterations.
- Assessment of ANLN expression in clinical thyroid cancer samples.
- In vitro functional assays (proliferation, migration, invasion) and in vivo xenograft models.
- Mechanistic studies including protein interaction and signaling pathway analysis.
Main Results:
- ANLN is upregulated in thyroid cancers, with higher expression linked to worse survival.
- ANLN promotes ATC cell proliferation, migration, and invasion.
- ANLN directly interacts with RhoA, activating the RhoA/PI3K/AKT pathway, driving tumor growth.
- Inhibition of AKT or RhoA suppressed ANLN-driven tumorigenic effects.
Conclusions:
- Anillin (ANLN) is a key driver of ATC progression.
- ANLN activates the RhoA/PI3K/AKT pathway, promoting tumor growth and metastasis.
- ANLN represents a potential therapeutic target for anaplastic thyroid cancer.
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