Long non-coding RNA LINC00460 promotes proliferation and inhibits apoptosis of cervical cancer cells by targeting microRNA-503-5p

• Published in: Molecular and cellular biochemistry 2020-12, Vol.475 (1-2), p.1-13
• Main Authors: Lin, Lin, Xin, Bing, Jiang, Tao, Wang, Xin-lu, Yang, Hua, Shi, Tie-mei
• Format: Article
• Language: English
• Subjects: Analysis; Annexin V; Apoptosis; Assaying; Biochemistry; Biomedical and Life Sciences; Cancer; Cardiology; Cell cycle; Cell growth; Cell proliferation; Cell viability; Cervical cancer; Cervix; Chromosome 5; Cycle protein; Flow cytometry; Gene expression; Health aspects; Immunohistochemistry; Kinases; Life Sciences; Medical Biochemistry; MicroRNA; miRNA; Non-coding RNA; Oncology; Pathogenesis; Protein binding; Proteins; Ribonucleic acid; RNA; Staining; Tissues; Tumors; Western blotting
• ISSN: 0300-8177; 1573-4919
• DOI: 10.1007/s11010-020-03853-0

Long non-coding RNAs are associated with the pathogenesis of cancers. Moreover, LINC00460 is involved in the development of multiple cancers. However, the function of LINC00460 in cervical cancer (CC) remains inconclusive. Herein, CC tissues and tumor-adjacent tissues were collected from patients. The effect of LINC00460 silencing in cell proliferation and apoptosis in CC was explored in vitro and in vivo. Additionally, the interaction between LINC00460 and miR-503-5p was analyzed using dual luciferase reporter assay. The expression of genes and proteins was assayed using quantitative real-time PCR, western blotting and immunohistochemistry, cell viability using MTT assay, cell cycle distribution using flow cytometry, cell apoptosis using Annexin V staining, Hoechst staining and TUNEL assay. LINC00460 levels in CC tissues were higher than tumor-adjacent tissues. LINC00460 silencing suppressed proliferation and promoted apoptosis of CC cells as evidenced by decreased cell viability, inhibited proliferation-related protein and cell cycle protein expressions and G1/S transition, increased apoptotic cells and Hoechst-positive cells, and enhanced apoptosis-related protein expressions. LINC00460 could bind to miR-503-5p and LINC00460 silencing enhanced miR-503-5p expression and inhibited its target gene expressions in CC cells. MiR-503-5p inhibition reversed LINC00460 silencing-caused inhibition of cell proliferation and miR-503-5p target gene expressions, and promotion of cell apoptosis. LINC00460 silencing also attenuated tumor growth, promoted miR-503-5p levels and cell apoptosis, and inhibited cell proliferation and miR-503-5p target gene expressions in tumor tissues. Hence, LINC00460 functioned as an oncogene in CC that affected cell proliferation and apoptosis via sponging miR-503-5p. This study provides a novel therapeutic target for CC.