FOXD3 regulates anaplastic thyroid cancer progression

Yin, Huabin; Meng, Tong; Zhou, Lei; Zhao, Feixing; Li, Xiufang; Li, Yundong; Hu, Meng-Jun; Chen, Haiyan; Song, Dianwen

doi:10.18632/oncotarget.16853

Cited by 7 publications

(7 citation statements)

References 23 publications

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“…it was reported that FoXd3 has an important role in the development of numerous cancers (29)(30)(31)(32)(33)(34)(35)(36)(37). in colon cancer, FoXd3 suppressed the invasive ability and inhibited the apoptosis of cells by inhibiting the epidermal growth factor receptor-ras-raf-mitogen activated protein kinase kinase (MeK)-erK signaling pathway, or regulating mir-214 expression and function (32,33).…”

Section: Discussionmentioning

confidence: 99%

“…FoXd3 is an important stem cell factor expressed in various types of stem cells and has an established role in development (28). Various studies have reported that FoXd3 is also involved in the development of a number of cancers (29)(30)(31)(32)(33)(34)(35)(36)(37); however, reports into its roles and mechanisms in Hcc are limited.…”

Section: Mir-425-5p Promotes Cell Proliferation Migration and Invasion By Directly Targeting Foxd3 In Hepatocellular Carcinoma Cellsmentioning

confidence: 99%

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miR‑425‑5p promotes cell proliferation, migration and invasion by directly targeting FOXD3 in hepatocellular carcinoma cells

Shang

Zhan

et al. 2019

Mol Med Report

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Micrornas (mirs) are important regulators of the tumorigenesis and metastasis of various cancers. in the present study, the roles and underlying mechanisms of mir-425-5p in the development of hepatocellular carcinoma (Hcc) were investigated. rT-qPcr analysis revealed that mir-425-5p was upregulated in Hcc tissues and cell lines. a functional study in vitro using MTT assays, colony formation and Transwell assays demonstrated that overexpression of mir-425-5p promoted the proliferation, migration, and invasion of Hcc cells, prevented cell apoptosis and accelerates the epithelial-mesenchymal transition process, whereas mir-425-5p knockdown induced opposing effects. a further mechanistic study revealed that forkhead box d3 (FoXd3) was a direct target of mir-425-5p, and gain-and loss-of-function of FoXd3 studies demonstrated that FoXd3 suppressed Hcc cell proliferation, migration, and invasion. Furthermore, rescue experiments revealed that overexpression of FoXd3 counteracted the positive effects of mir-425-5p on Hcc malignant behaviors. collectively, the present results demonstrated that mir-425-5p promoted Hcc cell proliferation, migration, and invasion by suppressing FoXd3 expression, potentially providing a novel target for the treatment of Hcc.

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Section: Discussionmentioning

confidence: 99%

Section: Mir-425-5p Promotes Cell Proliferation Migration and Invasion By Directly Targeting Foxd3 In Hepatocellular Carcinoma Cellsmentioning

confidence: 99%

miR‑425‑5p promotes cell proliferation, migration and invasion by directly targeting FOXD3 in hepatocellular carcinoma cells

Shang

Zhan

et al. 2019

Mol Med Report

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“…The expression of IGF‐1R and BRAF was significantly increased in nonsmall‐cell lung cancer when Foxd3 was knocked down [46]. The level of phosphorylated ERK (p‐ERK) was significantly increased in undifferentiated thyroid cancer cells lacking Foxd3 expression [36]. In HCC, Foxd3 inhibits cell proliferation and migration by the miR‐137‐AKT pathway [40].…”

Section: Discussionmentioning

confidence: 99%

FOXD3 and GAB2 as a pair of rivals antagonistically control hepatocellular carcinogenesis

et al. 2022

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Our previous study demonstrated that GAB2 promoted tumorigenesis in liver tissue and was a potential target for the treatment of hepatocellular carcinoma (HCC). Here, we identified that the tumour suppressor protein Forkhead box D3 (Foxd3) is a transcriptional repressor of the Gab2 gene. In human HCC cells, FOXD3 expression is low, but GAB2 expression is abundant. Increased Foxd3 expression inhibited the expression of Gab2 in a dose‐dependent manner. Ectopic expression of Foxd3 in HCC cells reduced Gab2‐mediated promotion of cell proliferation and migration in vitro. Foxd3 also inhibited Gab2‐stimulated phosphorylation of Jak2 and Stat3. Furthermore, the protein levels of Foxd3 and Gab2 had a clear negative correlation: Gab2 expression was induced, whereas Foxd3 expression was suppressed in most tumour tissues in mice with diethylnitrosamine (DEN)‐induced hepatocellular carcinoma. These results suggest that the tumour suppressor Foxd3 and tumour enhancer Gab2 mutually inhibit each other to synergistically control the occurrence of HCC, providing a novel mechanism for treating this disease.

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“…In the past decades, traditional and molecular biological techniques have been used to reveal ATC-related genes and pathways [5–7]. For instances, Yin et al found that the downregulated expression of the forkhead box D3 (FOXD3) transcription factor in ATC cells promoted invasiveness and epithelial-to-mesenchymal transition (EMT) and decreased cellular apoptosis.…”

Section: Introductionmentioning

confidence: 99%

“…For instances, Yin et al found that the downregulated expression of the forkhead box D3 (FOXD3) transcription factor in ATC cells promoted invasiveness and epithelial-to-mesenchymal transition (EMT) and decreased cellular apoptosis. FOXD3 silencing also enhanced p-ERK levels in the ATC cells, suggesting it negatively regulated MAPK/ERK signaling [5]. Zhang et al observed that S100A4 was highly expressed in ATC tissues.…”

Section: Introductionmentioning

confidence: 99%

Integrated Bioinformatics Analysis of Hub Genes and Pathways in Anaplastic Thyroid Carcinomas

Gao

Wang

Zhang

2019

International Journal of Endocrinology

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Anaplastic thyroid carcinoma (ATC) is a very rare malignancy; the pathogenesis of which is still not fully understood. The aim of the present study was to identify hub genes and pathways in ATC by microarray expression profiling. Two independent datasets (GSE27155 and GSE53072) were downloaded from GEO database. The differentially expressed genes (DEGs) between ATC tissues and normal thyroid tissues were screened out by the limma package and then enriched by gene ontology (GO) and KEGG pathway analysis. The hub genes were selected by protein-protein interaction (PPI) analysis. A total of 141 common upregulated and 87 common downregulated genes were screened out. These DEGs were significantly enriched in the phagosome and NF-kappa B signaling pathway. Through PPI analysis, TOP2A, TYMS, CCNB1, RACGAP1, FEN1, PRC1, and UBE2C were selected as hub genes, which were highly expressed in ATC tissues. TCGA data suggested that the expression levels of TOP2A, TYMS, FEN1, and PRC1 genes were also upregulated in other histological subtypes of thyroid carcinoma. High expression of TOP2A, TYMS, FEN1, PRC1, or UBE2C gene significantly decreased disease-free survival of patients with other thyroid carcinomas. In conclusion, the present study identified several hub genes and pathways, which will contribute to elucidating the pathogenesis of ATC and providing therapeutic targets for ATC.

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FOXD3 regulates anaplastic thyroid cancer progression

Cited by 7 publications

References 23 publications

miR‑425‑5p promotes cell proliferation, migration and invasion by directly targeting FOXD3 in hepatocellular carcinoma cells

miR‑425‑5p promotes cell proliferation, migration and invasion by directly targeting FOXD3 in hepatocellular carcinoma cells

FOXD3 and GAB2 as a pair of rivals antagonistically control hepatocellular carcinogenesis

Integrated Bioinformatics Analysis of Hub Genes and Pathways in Anaplastic Thyroid Carcinomas

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