Background 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. However, the role and regulatory mechanism of linc00887 in the progression of cervical cancer remain largely unknown. Methods In 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. Results Linc00887 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. Conclusions Linc00887, sponging miR-454-3p, inhibited the progression of cervical cancer by activating the FRMD6-Hippo signaling pathway.
Esophageal squamous cell carcinoma (ESCC) is a major type of esophageal cancer, accounting for about 90% of cases. Circular RNA UBAP2 (circUBAP2) is involved in the progression of several types of cancers. However, the role of circUBAP2 in ESCC remains unclear. In the present study, circUBAP2 expression was found to be upregulated in ESCC tumour tissues. Knockdown of circUBAP2 through infection with lentiviral vector encoding shRNA targeting circUBAP2 (sh-circUBAP2) inhibited the proliferation, migration and invasion of ESCC cells. In addition, circUBAP2 significantly promoted the proliferation, migration and invasion of ESCC cells. In vivo xenograft assay demonstrated that circUBAP2 downregulation suppressed the tumour growth of ESCC. Further mechanism investigations proved that circUBAP2 exerted its role via sponging microRNA (miR)-422a, and miR-422a directly targeted Rab10 in ESCC cells. These findings suggested that circUBAP2 acted as oncogene through regulating the miR-422a/Rab10 axis in ESCC. K E Y W O R D ScircUBAP2, esophageal squamous cell carcinoma (ESCC), miR-422a, oncogene, Rab10
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