Long non-coding RNA CATIP antisense RNA 1 (lncRNA CATIP-AS1) downregulation contributes to the progression and metastasis of thyroid cancer via epithelial-mesenchymal transition (EMT) pathway

Thyroid cancer (THCA) is the most common cancer of the endocrine system across the globe. To date, the mechanism of development of THCA remains scarcely known. In this study, we aim to elucidate the long non-coding RNA CATIP antisense RNA 1 (lncRNA CATIP-AS1/CATIP-AS1) role in the pathogenesis of THCA and its regulatory mechanism. The result shows that the CATIP-AS1 was significantly downregulated in THCA tissues and cells and was associated with a poor prognosis of patients diagnosed with THCA. The overexpression of CATIP-AS1 significantly inhibited THCA cell proliferation, migration, and epithelial-mesenchymal transition (EMT) but increased the THCA cell apoptosis. We found that CATIP-AS1 endogenously sponges miR-515-5p and its overexpression could inhibit miR-515-5p regulatory effect. Moreover, the overexpression of miR-515-5p repressed the Smad4 expression level, consequently reversed the inhibiting effect of overexpressed CATIP-AS1 on the proliferation, and migration of THCA cell. It also reversed the increased THCA cell apoptosis and the downregulated-CATIP-AS1-induced cell EMT inhibition. Summarily, we demonstrated that the CATIP-AS1 promotes the progression and metastasis of THCA via EMT pathway partly through regulating the miR-515-5p and Smad4 expression in THCA cell. The CATIP-AS1 could be a promising biomarker for early THCA detection and prognosis and a possible therapeutic target for its treatment.

Automated summary

This study elucidated the role of CATIP-AS1 in thyroid cancer progression and metastasis through the EMT pathway by regulating miR-515-5p and Smad4 expression in THCA cells. CATIP-AS1 could potentially serve as a promising biomarker for early detection and prognosis of THCA, as well as a possible therapeutic target.