Circ_LDLR promoted the development of papillary thyroid carcinoma via regulating miR-195-5p/LIPH axis [post]

2020 unpublished
Emerging studies have demonstrated that circular RNAs (circRNAs) are key regulators for tumorigenesis in cancers, including papillary thyroid carcinoma (PTC). In this study, we attempted to explore the effects of circ_LDLR on PTC. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was adopted to determine the levels of circ_LDLR, miR-195-5p and lipase H (LIPH). RNase R digestion assay and Actinomycin D assay were utilized to analyze the characteristics of circ_LDLR. Colony
more » ... c_LDLR. Colony formation assay and 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay were employed to evaluate cell proliferation. Western blot assay was used for the determination of protein levels. Flow cytometry analysis was applied to determine cell apoptosis. Transwell assay was performed to assess cell migration and invasion. Dual-luciferase reporter assay was used to verify the associations among circ_LDLR, miR-195-5p and LIPH. The murine xenograft model was constructed to explore the roles of circ_LDLR in vivo . Results: Compared to normal tissues and cells, circ_LDLR was upregulated in PTC tissues and cells. Silencing of circ_LDLR suppressed PTC cell colony formation, proliferation, migration and invasion and promoted apoptosis in vitro and hampered tumor growth in vivo. For mechanism investigation, circ_LDLR could regulate LIPH expression via sponging miR-195-5p. Moreover, miR-195-5p inhibition restored the effects of circ_LDLR knockdown on the malignant behaviors of PTC cells. MiR-195-5p overexpression inhibited PTC cell colony formation, proliferation, migration and invasion and facilitated apoptosis by targeting LIPH. Conclusion: Circ_LDLR knockdown decelerated PTC progression by regulating miR-195-5p/LIPH axis, which might provide a novel therapeutic target for PTC. Background Papillary thyroid carcinoma (PTC) is the most common and least malignant tumor, which accounted for about 85% of thyroid cancers [1]. Due to high degree of differentiation, slow tumor growth and good postoperative prognosis, the 10-year survival rate of PTC patients can reach more than 90% [2, 3]. Nevertheless, some PTC patients still have a poor prognosis for the aggressive characteristics, such as older age, large primary tumor, distant metastasis and lymph node metastasis [4]. Therefore, improving our understanding of the pathogenesis of PTC and identifying novel targets for PTC therapy
doi:10.21203/rs.3.rs-16903/v1 fatcat:jy6xmpjwtva3bjx6lxv23sbmoi