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

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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.