We investigated the effects of silencing the regulator of ribosome synthesis 1 (RRS1) gene on the proliferation, migration, and invasion of ovarian carcinoma cells, and its possible role in modulating signal transduction in these cells. Normal ovarian epithelial cell line IOSE80 was
used as a control. We examined the mRNA and protein level of RRS1 using qRT-PCR and western blot in control and ovarian carcinoma cells (SKOV-3, SW626, and CAOV3). RNA interference technology was used to knockdown RRS1 expression in CAOV3 cells. MTT was used to examine the proliferation of
these cells, while a Transwell assay was used to assay the cells’ migration and invasion abilities. Western blot was used to measure the levels of CyclinD1, P21, MMP-2, MMP-9, p-JAK2 and p-STAT3 proteins. In comparison with normal ovarian epithelial cells (IOSE80), RRS1 mRNA and protein
levels were increased in ovarian carcinoma cells (SKOV-3, SW626 and CAOV3) (P < 0.05). Because RRS1 levels were highest in CAOV3 cells, these cells were used for subsequent experiments. RRS1 gene expression was knocked down in CAOV3 cells, and in comparison with the negative control
group, siRNA-RRS1 cells exhibited decreased proliferation in the MTT assay after 48 h and 72 h (P < 0.05). These cells also exhibited reduced migration and invasion (P < 0.05). Further, siRNA-RRS1 cells exhibited reduced expression of CyclinD1, MMP-2, MMP-9, P-JAK2 and
P-STAT3 proteins (P < 0.05), while P21 protein levels were increased (P < 0.05). Silencing RRS1 expression inhibits the proliferation, migration, and invasion of ovarian carcinoma cells. This effect may be mediated by the inhibition of the STAT3 signaling pathway in these
cells.
LncRNA AWPPH promotes the proliferation, migration and invasion of ovarian carcinoma cells via activation of the Wnt/β‑catenin signaling pathway
