Research Paper Volume 12, Issue 21 pp 21129—21146

LINC00452 promotes ovarian carcinogenesis through increasing ROCK1 by sponging miR-501-3p and suppressing ubiquitin-mediated degradation


Figure 6. LINC00452 promotes xenograft tumor growth in vivo. (A) CaOV3 cancer cells with stable transfection of negative control lncRNA, LINC00452 as well as LINC00452 in combination with ROCK1-shRNA were subcutaneously injected into nude mice, respectively. PCR assay was performed to detect LINC00452, miR-501-3p and ROCK1 expression. (B) Tumor growth curves as recorded by measuring tumor volume. Overexpressing LINC00452 promoted tumor growth, which was abolished upon knockdown (KD) of ROCK1. *** p < 0.001 versus lncRNA-NC group. (C) Representative images showing xenograft tumors. (D) Immunohistochemistry results showing overexpressing LINC00452 promoted cell proliferation in tumors as indicated by more Ki67-positive cells. Knockdown (KD) of ROCK1 dramatically decreased number of Ki67-positive cells. (E) Diagram image showed that the carcinogenicity of LINC00452 is partially due to competitive sponging of miR-501-3p followed with release of repression on the ROCK1, a key effector in Rho signaling pathway. Irrespective of its miRNA sponge function, LINC00452 is capable of preventing ROCK1 protein from ubiquitin/proteasome-mediated degradation via their mutual physical interaction.