PDLIM7 Promotes Tumor Metastasis in Papillary Thyroid Carcinoma via Stabilizing Focal Adhesion Kinase Protein
Authors' conclusion
PDLIM7 function as an oncoprotein in PTC to promote metastasis, and a novel underlying mechanism is proposed that PDLIM7 keeps FAK protein from proteosome-dependent degradation.
Study context
- Population
- Patients with PTC at The Second Affiliated Hospital of Guilin Medical University (n=80) and 512 PTC samples from The Cancer Genome Atlas; PTC cell lines; TPC-1 xenografts80 patients + 512 TCGA samples
- Comparison
- PDLIM7 knockdown vs control in PTC cell lines and xenografts; PDLIM7 expression in PTC tissues
Methodological detailsin vitro functional assays, xenograft mouse model, clinical cohort and TCGA database analysis
- In vitro functional assays
- Xenograft mouse model
- Clinical cohort and TCGA database analysis
Main finding
As reported in the abstract
- PDLIM7 protein frequently upregulated in PTC tissues and cells; overexpression associated with advanced clinicopathological characteristics
- PDLIM7 knockdown inhibits proliferation, migration and invasion in PTC cell lines in vitro
- PDLIM7 knockdown hinders growth and metastasis of TPC-1 xenografts in vivo
- PDLIM7 colocalizes with focal adhesion kinase (FAK) and integrin alpha V (ITGAV); knockdown causes FA disassembly and proteosome-dependent FAK degradation
Original publication
PDLIM7 Promotes Tumor Metastasis in Papillary Thyroid Carcinoma via Stabilizing Focal Adhesion Kinase Protein. Thyroid. Published 20 February 2024. doi:10.
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