Transcriptional enhanced associate domain factor 1 regulates cortactin-binding protein 2 N-terminal-like to control cell apoptosis in thyroid cancer.

[OBJECTIVE] Understanding the molecular mechanisms underlying papillary thyroid carcinoma (PTC) is crucial for identifying drug targets. This research aims to elucidate molecular interactions between transcriptional enhanced associate domain factor 1 (TEAD1) and cortactin-binding protein 2 N-terminal-like (CTTNBP2NL) in PTC cells and assess their effect on cell proliferation, apoptosis, and clonogenicity.

[MATERIAL AND METHODS] Transcriptome data were used to identify differences in TEAD1 and CTTNBP2NL in PTC tissues. The correlation of gene expression with overall patient survival was analyzed. Laboratory experiments were conducted using thyroid papillary carcinoma 1 (TPC1) cells, where the overexpression of TEAD1 and the downregulation of CTTNBP2NL were manipulated. The regulatory dynamics between the two genes were confirmed through molecular biochemistry experiments. The effects on cell proliferation were evaluated using cell proliferation assays, and the impact on clonogenicity was assessed through colony formation assays.

[RESULTS] Significant differences in TEAD1 and CTTNBP2NL were observed in PTC, with both genes showing strong correlations with overall patient survival. In TPC1 cells, the overexpression of TEAD1 remarkably mitigated the negative effects caused by CTTNBP2NL downregulation, reduced cell proliferation, and increased apoptosis. Quantitative polymerase chain reaction and Western blot analyses confirmed the regulatory relationship between TEAD1 and CTTNBP2NL. The overexpression of TEAD1 markedly enhanced the proliferative capacity of cells, while silencing CTTNBP2NL resulted in diminished cell growth. Clonogenic assays revealed that TEAD1 promoted colony formation, indicating its role in boosting cell survival and proliferation.

[CONCLUSION] TEAD1 plays a critical compensatory role in PTC cells by alleviating the adverse effects of CTTNBP2NL deficiency, thereby promoting cell survival and growth. Hence, TEAD1 could serve as a potential therapeutic target.