ArticleJournal of clinical laboratory analysis2022
hsa_circ_0119412 overexpression promotes cervical cancer progression by targeting miR-217 to upregulate anterior gradient 2.
Article in Journal of clinical laboratory analysis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Hsa_circ_0119412 is a tumor promoter in hepatocellular carcinoma by inhibiting miR-526b-5p to upregulate STMN1.Cancer biology & therapy · 2023Article
- Hsa_circ_0119412 Contributes to Development of Retinoblastoma by Targeting miR-186-5p/ELK4 Axis.Molecular biotechnology · 2023Article
- hsa_circ_0119412 overexpression promotes cervical cancer progression by targeting miR-217 to upregulate anterior gradient 2.Journal of clinical laboratory analysis · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMounting evidence summarizes that circRNA is closely implicated in the development of numerous cancers. Our study aimed to investigate the role of circ_0119412 whose function was not explored in cervical cancer.
methodsRT-qPCR analysis was utilized for the expression analysis of circ_0119412, miR-217, and anterior gradient 2 (AGR2). CCK-8 assay, transwell assay, and MTT assay were employed to assess cell proliferation, migration, and adhesion, respectively. Animal study was performed to check the role of circ_0119412 in vivo. Bioinformatics analysis was applied to predict the downstream targets of circ_0119412. RIP assay was utilized to examine miRNAs potentially bound by circ_0119412. The interplays between miR-217 and circ_0119412 or AGR2 were validated by dual-luciferase reporter assay.
resultscirc_0119412 expression was highly enhanced in cervical tumor tissues and cancer cells. circ_0119412 overexpression aggravated cervical cancer cell proliferation, migration, and adhesion, and its overexpression was also conducive to tumor formation and growth in animal models. AGR2 was upregulated in cervical cancer by the public bioinformatics data. circ_0119412 bound to miR-217, and miR-217 bound to AGR 3'UTR. The promoting effects of circ_0119412 overexpression on cancer cell malignant phenotypes were reversed by miR-217 enrichment. In addition, increased expression of miR-217 suppressed AGR2 expression, thus weakening the functional effects of AGR2.
conclusioncirc_0119412 functioned as an oncogenic driver to promote the malignant development of cervical cancer by targeting the miR-217/AGR2 pathway.
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