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

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Abstract

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.

Related collections

Most cited references 40

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Author and article information

Journal

Journal ID (nlm-ta): Endocr Connect

Journal ID (iso-abbrev): Endocr Connect

Journal ID (hwp): EC

Title: Endocrine Connections

Publisher: Bioscientifica Ltd (Bristol )

ISSN (Electronic): 2049-3614

Publication date (Electronic): 07 May 2024

Publication date (Electronic preprint): 11 April 2024

Publication date Collection: 01 June 2024

Volume: 13

Issue: 6

Electronic Location Identifier: e240034

Affiliations

[1 ]Department of Endocrinology and Diabetes Center , The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

[2 ]Zhongshan School of Medicine , Sun Yat-sen University, Guangzhou, China

Author notes

Correspondence should be addressed to Y Li or H Guan: liyb@ 123456mail.sysu.edu.cn or ghongy@ 123456mail.sysu.edu.cn

^*(W Liang and Y Zhang contributed equally to this work)

Author information

Yanbing Li http://orcid.org/0000-0003-3782-9210

Article

Publisher ID: EC-24-0034

DOI: 10.1530/EC-24-0034

PMC ID: 11103747

PubMed ID: 38614124

SO-VID: 15ec2bef-9048-4688-abd1-d72d6644016b

License:

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

History

Date received : 26 January 2024

Date accepted : 11 April 2024

Funding

Funded by: National Natural Science Foundation of China, doi http://dx.doi.org/10.13039/501100001809;

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