Background: The incidence of thyroid cancer continues to rise all over the world. Thus, it is urgent to find a novel strategy for the treatment of thyroid cancer. Previous reports have confirmed that lncRNA CASC2 is involved in the pathogenesis of thyroid cancer. However, the mechanism by which CASC2 mediates the tumorigenesis of thyroid cancer remains unclear.
Methods: Gene and protein expressions in tissues or cells were detected by q-PCR and Western blot, respectively. Cell proliferation was tested by MTT assay. Flow cytometry was used to test cell apoptosis. Cell migration and invasion in thyroid cancer cells was detected by transwell assay. In addition, the correlation between CASC2 and miR-24-3p were investigated by Targetscan and dual-luciferase reporter assay. Finally, xenograft mice model was established to detect the effect of CASC2 on thyroid cancer in vivo.
Results: CASC2 was significantly downregulated in thyroid cancer. Overexpression of CASC2 inhibited the proliferation, migration, and invasion of thyroid cancer cells. In addition, upregulation of CASC2 could inhibit the tumorigenesis of TC via sponging miR-24-3p. Furthermore, overexpression of CASC2 significantly suppressed the growth of thyroid cancer in vivo.
Conclusion: Overexpression of CCASC2 inhibits the tumorigenesis of thyroid cancer in vitro and in vivo. Thus, CASC2 may serve as a novel target for the treatment of thyroid cancer.
Keywords: CASC2; miR-24; thyroid cancer.
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