Long non‑coding RNA miR155HG silencing restrains ovarian cancer progression by targeting the microRNA‑155‑5p/tyrosinase‑related protein 1 axis
- Aiping Wen
- Le Luo
- Chengchao Du
- Xin Luo
Affiliations: Department of Gynecology and Obstetrics, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, P.R. China, Sichuan Key Laboratory of Medical Imaging, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, P.R. China, Department of Gynecology and Obstetrics, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, P.R. China
- Published online on: August 31, 2021 https://doi.org/10.3892/etm.2021.10672
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Ovarian cancer (OC) is the third commonest gynecological malignancy worldwide. The long non‑coding (lnc)RNA microRNA (miR)155HG functions as an oncogene in different human cancers. However, the function and molecular mechanism of miR155HG in OC remain elusive. The present study indicated that the expression levels of miR155HG and tyrosinase‑related protein 1 (TYRP1) were significantly increased, whereas that of miR155‑5p was decreased in OC tissues and cells, as detected by real‑time quantitative polymerase chain reaction. It was demonstrated that knockdown of miR155HG markedly inhibited OC cell viability, migration and invasion while promoting apoptosis, as indicated by 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide, wound healing, Transwell and western blot assays. Mechanistically, it was revealed that miR155HG and TYRP1 were both targeted by miR‑155‑5p with complementary binding sites in the 3' untranslated region. A dual‑luciferase reporter assay was used to confirm the targeting relationship between miR155HG, miR‑155‑5p and TYRP1. In addition, the interaction between miR155HG and miR‑155‑5p was further demonstrated by radioimmunoprecipitation and pull‑down assays. In addition, feedback approaches determined that miR‑155‑5p inhibition or TYRP1 overexpression markedly reversed the inhibitory effects of miR155HG knockdown on OC cell viability, migration and invasion as well as weakened the promotive effect of miR155HG knockdown on OC cell apoptosis. Thus, miR155HG silencing inhibited the malignant biological behavior of OC cells by targeting the miR‑155‑5p/TYRP1 axis. The present study provides novel insights into the underlying mechanism of OC progression.