microRNA-29c inhibits cell proliferation by targeting NASP in human gastric cancer.

Abstract

BACKGROUND:

Gastric cancer is one of the most common malignancies worldwide. Recent studies have shown that microRNAs play crucial roles in regulating cellular proliferation process in gastric cancer. MicroRNA-29c (miR-29c) acts as a tumor suppressor in different kinds of tumors.

METHODS:

Quantitative PCR was performed to evaluate miR-29c expression level in 67 patient gastric cancer tissues and 9 gastric cancer cell lines. The effects of miR-29c were explored by proliferation assay, soft agar colony formation assay, apoptosis and cell cycle analysis using flow cytometry. The target gene was predicted by bioinformatic algorithms and validated by dual luciferase reporter assay and Western blot analysis.

RESULTS:

In this study, we demonstrate that miR-29c is down-regulated in gastric cancer tissues and cell lines. We indicate that overexpression of miR-29c inhibits cell proliferation, promotes apoptosis and arrests cell cycle at G1/G0 phase. We additionally show that miR-29c exerts these effects by targeting Nuclear autoantigenic sperm protein (NASP). Moreover, depletion of NASP can elite the phenotypes caused by miR-29c.

CONCLUSIONS:

These data suggest that miR-29c inhibits proliferation in gastric cancer and could potentially serve as an early biomarker and a novel therapy target.

• Authors: Beiqin Yu, Xuehua Chen, Jianfang Li, Qinlong Gu, Zhenggang Zhu, Chen Li, Liping Su, Bingya Liu
• Journal: BMC cancer (BMC Cancer) Vol. 17 Issue 1 Pg. 109 (Feb 07 2017) ISSN: 1471-2407 [Electronic] England
• PMID: 28173777 (Publication Type: Journal Article)

Chemical References

• Autoantigens
• MIRN29a microRNA, human
• MicroRNAs
• NASP protein, human
• Nuclear Proteins

Topics

• Animals
• Apoptosis
• Autoantigens (genetics, metabolism, physiology)
• Cell Line, Tumor
• Cell Proliferation
• Down-Regulation
• Gene Expression Regulation, Neoplastic
• Humans
• Mice
• MicroRNAs (genetics, metabolism, physiology)
• Nuclear Proteins (genetics, metabolism, physiology)
• Signal Transduction
• Stomach Neoplasms (genetics, metabolism, physiopathology)
• Xenograft Model Antitumor Assays