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FLNA overexpression promotes papillary thyroid cancer aggression via the FAK/AKT signaling pathway

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Title: FLNA overexpression promotes papillary thyroid cancer aggression via the FAK/AKT signaling pathway
Authors: Weiwei Liang, Yilin Zhang, Yan Guo, Pengyuan Zhang, Jiewen Jin, Hongyu Guan, Yanbing Li
Source: Endocrine Connections, Vol 13, Iss 6, Pp 1-11 (2024)
Publisher Information: Bioscientifica, 2024.
Publication Year: 2024
Collection: LCC:Diseases of the endocrine glands. Clinical endocrinology
Subject Terms: flna, invasion, migration, papillary thyroid cancer, fak/akt pathway, Diseases of the endocrine glands. Clinical endocrinology, RC648-665
More Details: Background: Filamin A (FLNA) is a member of the filamin family and has been found to be critical for the progression of several cancers. However, its biological function in papillary thyroid cancer (PTC) remains largely unexplored. Methods: Data from The Cancer Genome Atlas (TCGA) databases were utilized to analyze the FLNA expression level and its influence on the clinical implications of patients with PTC. Gene Expression Omnibus (GEO) and qRT-PCR was used to verify the expression levels of FLNA in PTC. Kaplan–Meier survival analysis was conducted to evaluate the prognostic value of FLNA in PTC. Transwell assays and wound healing were performed to examine the biological function of FLNA knockdown in PTC cells. Gene set enrichment analysis (GSEA) and Western blotting were conducted to investigate the potential mechanisms underlying the role of FLNA in PTC progression. In addition, the relationship between FLNA expression and the tumor immune microenvironment (TME) in PTC was explored. Results: FLNA was significantly upregulated in PTC tissues. High expression levels of FLNA was correlated with advanced TNM stage, T stage, and N stage, as well as poor disease-free interval (DFI) and progression-free interval (PFI) time in PTC patients. Moreover, we found that FLNA knockdown inhibited the migration and invasion of PTC cells. Mechanistically, FLNA knockdown inhibited epithelial–mesenchymal transition (EMT) in PTC and affected the activation of the FAK/AKT signaling pathway. In addition, FLNA expression was associated with TME in PTC. Conclusion: FLNA may be regarded as a new therapeutic target for PTC patients.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2049-3614
Relation: https://ec.bioscientifica.com/view/journals/ec/13/6/EC-24-0034.xml; https://doaj.org/toc/2049-3614
DOI: 10.1530/EC-24-0034
Access URL: https://doaj.org/article/2117a0632a8b4d0094b14eaaf04aea31
Accession Number: edsdoj.2117a0632a8b4d0094b14eaaf04aea31
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  Data: FLNA overexpression promotes papillary thyroid cancer aggression via the FAK/AKT signaling pathway
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  Data: <searchLink fieldCode="AR" term="%22Weiwei+Liang%22">Weiwei Liang</searchLink><br /><searchLink fieldCode="AR" term="%22Yilin+Zhang%22">Yilin Zhang</searchLink><br /><searchLink fieldCode="AR" term="%22Yan+Guo%22">Yan Guo</searchLink><br /><searchLink fieldCode="AR" term="%22Pengyuan+Zhang%22">Pengyuan Zhang</searchLink><br /><searchLink fieldCode="AR" term="%22Jiewen+Jin%22">Jiewen Jin</searchLink><br /><searchLink fieldCode="AR" term="%22Hongyu+Guan%22">Hongyu Guan</searchLink><br /><searchLink fieldCode="AR" term="%22Yanbing+Li%22">Yanbing Li</searchLink>
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  Data: Endocrine Connections, Vol 13, Iss 6, Pp 1-11 (2024)
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  Data: Bioscientifica, 2024.
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  Data: 2024
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  Data: LCC:Diseases of the endocrine glands. Clinical endocrinology
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  Data: <searchLink fieldCode="DE" term="%22flna%22">flna</searchLink><br /><searchLink fieldCode="DE" term="%22invasion%22">invasion</searchLink><br /><searchLink fieldCode="DE" term="%22migration%22">migration</searchLink><br /><searchLink fieldCode="DE" term="%22papillary+thyroid+cancer%22">papillary thyroid cancer</searchLink><br /><searchLink fieldCode="DE" term="%22fak%2Fakt+pathway%22">fak/akt pathway</searchLink><br /><searchLink fieldCode="DE" term="%22Diseases+of+the+endocrine+glands%2E+Clinical+endocrinology%22">Diseases of the endocrine glands. Clinical endocrinology</searchLink><br /><searchLink fieldCode="DE" term="%22RC648-665%22">RC648-665</searchLink>
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  Label: Description
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  Data: Background: Filamin A (FLNA) is a member of the filamin family and has been found to be critical for the progression of several cancers. However, its biological function in papillary thyroid cancer (PTC) remains largely unexplored. Methods: Data from The Cancer Genome Atlas (TCGA) databases were utilized to analyze the FLNA expression level and its influence on the clinical implications of patients with PTC. Gene Expression Omnibus (GEO) and qRT-PCR was used to verify the expression levels of FLNA in PTC. Kaplan–Meier survival analysis was conducted to evaluate the prognostic value of FLNA in PTC. Transwell assays and wound healing were performed to examine the biological function of FLNA knockdown in PTC cells. Gene set enrichment analysis (GSEA) and Western blotting were conducted to investigate the potential mechanisms underlying the role of FLNA in PTC progression. In addition, the relationship between FLNA expression and the tumor immune microenvironment (TME) in PTC was explored. Results: FLNA was significantly upregulated in PTC tissues. High expression levels of FLNA was correlated with advanced TNM stage, T stage, and N stage, as well as poor disease-free interval (DFI) and progression-free interval (PFI) time in PTC patients. Moreover, we found that FLNA knockdown inhibited the migration and invasion of PTC cells. Mechanistically, FLNA knockdown inhibited epithelial–mesenchymal transition (EMT) in PTC and affected the activation of the FAK/AKT signaling pathway. In addition, FLNA expression was associated with TME in PTC. Conclusion: FLNA may be regarded as a new therapeutic target for PTC patients.
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