MicroRNA miR-425 promotes tumor progression by inhibiting Dickkopf-related protein-3 in gastric cancer

ABSTRACT

Gastric cancer is a prevalent yet heterogeneous disease which ranks as the fifth most common cancer in the world. Dietary habit, genetic background, Helicobacter Pylori infections were the risk factors of gastric cancer. MicroRNA miR-425 is highly expressed in gastric cancer, but little attention has been devoted to the mechanism of miR-425 in tumorigenesis. This study aim to investigate the role of miR-425 in gastric cancer.

The expression of miR-425 and Dickkopf-related protein-3(DKK-3) were analyzed by qRT-PCR. Gastric cell line BGC-823 and SGC-7901 were transfected miR-425 inhibitors or NC. Then, cell viability was determined by CCK-8, cell apoptosis and cell cycle were assessed by flow cytometer. Cell migration and cell invasion were analyzed by wound healing and trans-well assays. Luciferase reporter assay was conducted to assess the correlation between miR-425 and DKK-3. Downstream regulators, such as p-ASK1 and p-JNK, were analysis by western blot.

Compared with normal gastric epithelium cell line, miR-425 was obviously upregulated in gastric cancer cell lines. MiR-425 inhibitor suppressed the cell viability, cell migration and cell invasion. The Luciferase assay data identified that DKK-3 is a target of miR-425. While miR-425 could lower the expression of DKK-3 which mediate tumorigenesis in a certain way.

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KEYWORDS:

• MiR-425
• DKK-3
• gastric cancer
• oncogene

Highlights:

MiR-425 was obviously upregulated in gastric cell lines.+

Downregulation of miR-425 could inhibit the cell proliferation and migration.

DKK-3 is a direct target of miR-425, involved in mediating of JNK/MAPK signaling pathway.

Disclosure of potential conflicts of interest

No potential conflict of interest was reported by the author(s).

Supplementary material

Supplemental data for this article can be accessed here.