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CircPIP5K1A facilitates gastric cancer progression via miR-376c-3p/ZNF146 axis.
Ma, Yan; Cong, Xiliang; Zhang, Yiyun; Yin, Xin; Zhu, Ziyu; Xue, Yingwei.
Afiliação
  • Ma Y; 1Department of Gastroenterological Surgery, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081 China.
  • Cong X; 1Department of Gastroenterological Surgery, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081 China.
  • Zhang Y; 2Department of Endoscopy, Harbin Medical University Cancer Hospital, 150 HaPing Road, Harbin, 150081 China.
  • Yin X; 1Department of Gastroenterological Surgery, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081 China.
  • Zhu Z; 1Department of Gastroenterological Surgery, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081 China.
  • Xue Y; 1Department of Gastroenterological Surgery, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081 China.
Cancer Cell Int ; 20: 81, 2020.
Article em En | MEDLINE | ID: mdl-32190005
ABSTRACT

BACKGROUND:

Recently, many emerging circular RNAs (circRNAs) have been studied in human malignancies, including gastric cancer (GC). Researches concerning cancers have revealed that aberrant expression of circRNAs play a big part in tumorigenesis and development of diverse malignant tumors. Although hsa_circ_0014130 (circPIP5K1A) has been confirmed to be closely related to non-small cell lung cancer (NSCLC) progression, the knowledge of its function on GC progression remains unclear. Therefore, it is of great interest to uncover the underlying role of circPIP5K1A in GC.

METHODS:

The expression and characteristic of circPIP5K1A were separately analyzed by RT-qPCR, nucleic acid electrophoresis, RNase R and Actinomycin D treatment. CCK-8, colony formation, EdU, transwell, TUNEL, flow cytometry, luciferase reporter, RIP and RNA pull-down assays were employed to testify the regulatory role of circPIP5K1A in GC.

RESULTS:

In current study, circPIP5K1A, featured with closed-loop structure, was proved to be highly expressed in tissues and cells of GC. Loss-of-function assays depicted that silencing circPIP5K1A suppressed GC development. Follow-up mechanism tests unveiled that circPIP5K1A bound with miR-376c-3p and inhibition of miR-376c-3p reversed circPIP5K1A downregulation-mediated effect on GC progression. Additionally, ZNF146 was verified to be the downstream molecule of circPIP5K1A/miR-376c-3p axis in modulating GC progression.

CONCLUSIONS:

circPIP5K1A stimulates GC progression by sponging miR-376c-3p to upregulate ZNF146 expression.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Revista: Cancer Cell Int Ano de publicação: 2020 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Revista: Cancer Cell Int Ano de publicação: 2020 Tipo de documento: Article