Abstract
BackgroundEmerging evidence suggested that long intergenic noncoding RNA (lincRNA) 00887 (NR_024480) reduced the invasion and metastasis of non-small cell lung cancer by sponging miRNAs degradation. However, the role and regulatory mechanism of linc00887 in the progression of cervical cancer remain largely unknown.MethodsIn vivo or vitro, RT-qPCR assay was used to detect the expression of linc00887 in human normal (N = 30), cervical cancer tissues (N = 30), human normal cervical epithelial cells (Ect1/E6E7) and cervical cancer cell lines (HeLa, C33A). Then, CCK-8 and Transwell assays were used to examine cell proliferation and invasion when linc00887 was overexpressed or knocked down. In addition, bioinformatics, luciferase reporter gene and pull-down assays were used to predict and validate the relationship between linc00887 and miR-454-3p. Moreover, we detected the expression of miR-454-3p in Ect1/E6E7, HeLa and C33A cells when linc00887 was overexpressed or knocked down. Cell proliferation and invasion were also measured when pcDNA-linc00887 and miR-454-3p were transfected alone or together. Next, miR-454-3p target gene was predicted and validated by bioinformatics and luciferase reporter gene assays. Gain- and loss-of-function experiments were performed in HeLa cells to evaluate the effect of miR-454-3p or linc00887 on the expression of FERM domain containing protein 6 (FRMD6) protein and several key proteins in the FRMD6-Hippo signaling pathway.ResultsLinc00887 was downregulated in cervical cancer tissues or human cervical cancer cell lines (Hela, C33A) compared with normal tissues or cell lines. Overexpression of linc00887 inhibited proliferation and invasion HeLa and C33A cells, while linc00887 knockdown had the opposite effect. Linc00887 bound with miR-454-3p, and overexpression of miR-454-3p rescued linc00887-induced inhibition proliferation and invasion of HeLa cells. MiR-454-3p targeted and suppressed the expression of FRMD6, and linc00887 suppressed tumorigenesis of cervical cancer through activating the FRMD6-Hippo signaling pathway.ConclusionsLinc00887, sponging miR-454-3p, inhibited the progression of cervical cancer by activating the FRMD6-Hippo signaling pathway.
Highlights
Emerging evidence suggested that long intergenic noncoding RNA 00887 (NR_024480) reduced the invasion and metastasis of non-small cell lung cancer by sponging miRNAs degradation
We selected five cervical cancer cell lines (Hela, C33A, Caski, ME180 and Siha) to examine the linc00887 level in vitro, which were detected by RT-qPCR
The results showed that linc00887 level was downregulated in cervical cancer cell lines, especially in HeLa and C33A cell lines, compared with normal cervical cell lines (Ect1/E6E7) (p < 0.05) (Fig. 1b)
Summary
Emerging evidence suggested that long intergenic noncoding RNA (lincRNA) 00887 (NR_024480) reduced the invasion and metastasis of non-small cell lung cancer by sponging miRNAs degradation. Cervical cancer is a common female malignant tumor [1], and there is no effective treatment at present. Li et al Cancer Cell Int (2021) 21:33 about 30,400 in China in 2014, with a crude mortality rate of 4.57/100,000 [4]. Cervical intraepithelial neoplasia (CIN) is a sign of cervical lesions, and screening can help the treatment of cervical cancer. Previous studies reported that pretreatment of cervical cancer cells with proteasome inhibitor MG132 promotes bystander killing mediated by chemotherapy drug mitomycin C [6]. Bevacizumab, an antiangiogenic agent targeting vascular endothelial growth factor 2 (VEGF-2), is added to standard chemotherapy for cervical cancer to improve survival [7, 8]. Early prevention and treatment of cervical cancer is important
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