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Hsa_Circ_0001947/MiR-661/DOK7 Axis Restrains Non-Small Cell Lung Cancer Development

  • Bao, Yuyan (Pharmaceutical Preparation Section, Sanmen People's Hospital) ;
  • Yu, Yanjie (Sanmen Market Supervisory Authority) ;
  • Hong, Bing (Pharmaceutical Preparation Section, Sanmen People's Hospital) ;
  • Lin, Zhenjian (Pharmaceutical Preparation Section, Sanmen People's Hospital) ;
  • Qi, Guoli (Pharmaceutical Preparation Section, Sanmen People's Hospital) ;
  • Zhou, Jie (Pharmaceutical Preparation Section, Sanmen People's Hospital) ;
  • Liu, Kaiping (Pharmaceutical Preparation Section, Sanmen People's Hospital) ;
  • Zhang, Xiaomin (Pharmaceutical Preparation Section, Sanmen People's Hospital)
  • Received : 2021.06.11
  • Accepted : 2021.09.09
  • Published : 2021.11.28

Abstract

Hsa_circ_0001947 is associated with multiple cancers, but its function in non-small cell lung cancer (NSCLC) is ambiguous and needs further research. The targeting relationship among circ_0001947, miR-661, and downstream of tyrosine kinase 7 (DOK7) was predicted by database and further verified by dual-luciferase reporter assay, while their expressions in cancer tissues and cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR). After transfection, cell biological behaviors and expressions of miRNAs, miR-661 and DOK7 were determined by cell function experiments and qRT-PCR, respectively. Circ_0001947 was low-expressed in NSCLC tissues and cells. Circ_0001947 knockdown intensified cell viability and proliferation, induced cell cycle arrest at S phase, suppressed apoptosis and evidently enhanced miR-510, miR-587, miR-661 and miR-942 levels, while circ_0001947 overexpression did the opposite. MiR-661 was a target gene of circ_0001947 that participated in the regulation of circ_0001947 on cell biological behaviors. Furthermore, DOK7, the target gene of miR-661, partly participated in the regulation of miR-661 on cell viability. Hsa_circ_0001947 acts as a sponge of miR-661 to repress NSCLC development by elevating the expression of DOK7.

Keywords

Acknowledgement

This work was supported by Joint Fund Project of Zhejiang Provincial Natural Science Foundation and Pharmaceutical Association [Grant Number: LYY19H310004] and Zhejiang Medical and Health Science and Technology Plan Project [Grant Number: 2018KY183].

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