LINC00115 has been documented to regulate many different cancers; however, its function in thyroid cancer (THCA) remains unexplored. Therefore, we examined the effects of LINC00115 on THCA and the associated molecular mechanisms. In THCA cell lines and tumor samples, the expression levels of LINC00115, miR-489-3p, and EVA1A were analyzed by qRT-PCR along with respective controls. Cell viability, migration, and apoptosis were analyzed by employing CCK-8, transwell, and western blotting assays, respectively. Xenograft experiments were done to assess in vivo tumor growth. The interaction among LINC00115, miR-489-3p, and EVA1A was tested using RNA-binding protein immunoprecipitation and luciferase assays. Key proteins of the Hippo signaling pathway were ascertained by western blotting. The outcomes elucidated that LINC00115 was overexpressed in THCA cell lines and tumor tissues. LIN00115 knockdown reduced in vitro proliferation and migration but facilitated apoptosis in THCA cells and inhibited in vivo tumor growth. The target of LINC00115 was miR-489-3p, which binds to EVA1A in THCA. Functional assays revealed that miR-489-3p inhibition boosted THCA cell proliferation and migration, but hindered apoptosis. However, EVA1A knockdown resulted in the opposite effects via the Hippo signaling pathway. Additionally, miR-489-3p inhibition partially negated the effects of LINC00115 knockdown in THCA cells, and EVA1A knockdown remarkably impeded the effects of miR-489-3p inhibition in THCA cells. Thus, LINC00115 knockdown suppressed THCA carcinogenesis via targeting miR-489-3p, which regulates EVA1A expression and affects the Hippo signaling pathway.
Keywords: EVA1A; LINC00115; Thyroid cancer; microRNA-489-3p.
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