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Circular RNA HIPK3 plays a carcinogenic role in cervical cancer progression via regulating miR-485-3p/FGF2 axis
  1. Shanshan Wu1,
  2. Shimei Liu2,
  3. Huaihua Song2,
  4. Jiayu Xia1
  1. 1 Obstetrics and Gynecology, Linyi Central Hospital, Linyi, Shandong, China
  2. 2 Obstetrics and Gynecology, The Third People's Hospital of Linyi, Linyi, Shandong, China
  1. Correspondence to Dr Jiayu Xia, Obstetrics and Gynecology, Linyi Cancer Hospital, Linyi 276000, China; tjfxzx{at}126.com

Abstract

Circular RNA (circRNA) is an endogenous RNA molecule with a stable closed-loop structure. The circular RNA HIPK3 (circHIPK3) is highly expressed in hepatocellular carcinoma and facilitates tumor growth. However, its role in cervical cancer (CC) and its regulatory mechanisms are not well-studied. This study aimed for investigating the function of circHIPK3 on proliferation and metastasis of CC cells. In this study, quantitative real-time PCR assay was adopted to delve into the circHIPK3 expression in CC cell lines. Cell counting kit-8 and colony formation assays were used to evaluate the influence of overexpression and knockdown of circHIPK3 on CC cell proliferation. Dual-luciferase reporter assay was employed to probe into the binding of miR-485-3p to circHIPK3 and miR-485-3p to the 3’ untranslated region (UTR) of fibroblast growth factor 2 (FGF2), respectively. FGF2 protein expression was detected by western blot analysis. This study confirmed that circHIPK3 was highly expressed in CC tissues. Overexpressed circHIPK3 could remarkably expedite the proliferation, migration and invasion of SiHa cells, and knocking down circHIPK3 could significantly impede the proliferation, migration and invasion of HeLa cells. MiR-485-3p can directly bind to circHIPK3 and the 3’UTR of FGF2. Overexpression of circHIPK3 triggered the upregulation of FGF2 expression while knockdown of circHIPK3 reduced FGF2 expression in CC cells, and the transfection of miR-485-3p mimics reversed the upregulation of FGF2 expression and enhanced malignant phenotypes in CC cells with overexpressed circHIPK3.

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Footnotes

  • Contributors Conceived and designed the experiments: XZ. Performed the experiments: SW, SL, HS. Statistical analysis: HS. Wrote the paper: SW. All authors read and approved the final manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Ethics approval This study was backed by the Ethics Review Board of Linyi Central Hospital (Approval ID: 201 604d005). All the patients involved signed a consent form.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data availability statement The data used to support the findings are available from the corresponding author on reasonable request.

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