LINC00092 Enhances LPP Expression to Repress Thyroid Cancer Development via Sponging miR-542-3p

Abstract

AbstractLINC00092 is poorly expressed in Thyroid cancer (TC), while its role in TC tumorigenesis is still elusive. This study aimed to reveal the role and regulatory mechanism of LINC00092 in TC.RNA immunoprecipitation and dual luciferase reporter assays were employed to ascertain the relationships among lipoma preferred partner (LPP), miR-542-3p, and LINC00092. qRT-PCR analysis was performed to detect their expression levels in TC. LPP protein productions were evaluated via western blotting. CCK-8, transwell, and colony formation assays were done to estimate TC cells’ biological functions. A murine xenograft model was built to observe tumor formation in vivo.LINC00092 overexpression decreased the expression levels of miR-542-3p, and LPP was targeted by miR-542-3p. In TC cells and tissues, the elevation of miR-542-3p, and low amounts of LINC00092 and LPP can be observed. Both LINC00092 and SPAG6 were considered as the antineoplastic factors in TC since their overexpression dramatically repressed TC cells’ invasive and proliferative potentials, while miR-542-3p exerted the opposite functions in TC. The ectopic expression of LINC00092 also suppressed tumor growth in vivo. In addition, it revealed that miR-542-3p upregulation reversed LINC00092 overexpression-mediated effects on TC cells. At the same time, the enhanced influences of TC cells caused by miR-542-3p upregulation could be attenuated by the enforced LPP.This study innovatively reveals that LINC00092 acts as an antineoplastic lncRNA to restrain the development of TC via regulating miR-542-3p/LPP. The findings of this study may provide a prospective drug target on LINC00092/miR-542-3p/LPP axis for the treatment of TC.