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miR-1236-3p inhibits invasion and metastasis in gastric cancer by targeting MTA2.
An, Jia-Xiang; Ma, Ming-Hui; Zhang, Chun-Dong; Shao, Shuai; Zhou, Nuo-Ming; Dai, Dong-Qiu.
Afiliación
  • An JX; Department of Gastroenterological Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, 110032 China.
  • Ma MH; Department of Gastroenterological Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, 110032 China.
  • Zhang CD; Department of Gastroenterological Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, 110032 China.
  • Shao S; Department of Gastroenterological Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, 110032 China.
  • Zhou NM; Department of Gastroenterological Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, 110032 China.
  • Dai DQ; Department of Gastroenterological Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, 110032 China.
Cancer Cell Int ; 18: 66, 2018.
Article en En | MEDLINE | ID: mdl-29743816
ABSTRACT

BACKGROUND:

MicroRNAs deregulation are common in human tumor progression. miR-1236-3p has been reported to function as tumor suppressor microRNA in various malignancies. The aim of this study was to demonstrate the downregulated expression of miR-1236-3p in gastric cancer (GC) tissues and cell lines, and clarify its biological function in GC.

METHODS:

Real-time polymerase chain reaction was used to measure the mRNA level of miR-1236-3p in GC. Dual luciferase assay was used to demonstrate that MTA2 was one of the candidate target genes of miR-1236-3p. Western blots were utilized to detect the protein levels. Cell function assays were also performed to determine the function of miR-1236-3p in GC.

RESULTS:

miR-1236-3p expression, which was associated with lymph node metastasis, differentiation and clinical stage, was significantly reduced in GC tissues and cell lines. miR-1236-3p over-expression could inhibit GC cell proliferation, migration and invasion, and inhibition of miR-1236-3p expression had opposite effects. Furthermore, we demonstrated that MTA2 was a candidate target of miR-1236-3p, and miR-1236-3p over-expression significantly inhibited the process of epithelial-mesenchymal transition. We also found that miR-1236-3p could suppress the PI3K/Akt signaling pathway in GC cells.

CONCLUSIONS:

Our results suggest that miR-1236-3p functions as a tumor suppressor in GC and could be a promising therapeutic target for GC.
Palabras clave

Texto completo: 1 Banco de datos: MEDLINE Idioma: En Revista: Cancer Cell Int Año: 2018 Tipo del documento: Article

Texto completo: 1 Banco de datos: MEDLINE Idioma: En Revista: Cancer Cell Int Año: 2018 Tipo del documento: Article