miR-22 is down-regulated in gastric cancer, and its overexpression inhibits cell migration and invasion via targeting transcription factor Sp1

被引:0
|
作者
Mei-Mei Guo
Li-Hua Hu
Yong-Qiang Wang
Peng Chen
Jian-Guo Huang
Ning Lu
Jiang-Hong He
Cheng-Gong Liao
机构
[1] Shenzhen Sixth People’s Hospital (Nanshan Hospital),Department of Gastroenterology
[2] Heilongjiang Provincial Hospital,Department of Gastroenterology
[3] Cancer Hospital of Xinjiang Medical University,Department of Medicine
[4] Urumqi General Hospital of Lanzhou Military Command of PLA,Department of Oncology
来源
Medical Oncology | 2013年 / 30卷
关键词
miR-22; Gastric cancer; Invasion; Migration; Sp1;
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学科分类号
摘要
Accumulating evidence has shown that microRNAs are involved in multiple processes in cancer development and progression. Recently, miR-22 has been identified as a tumor-suppressing microRNA in many human cancers. However, the specific function of miR-22 in gastric cancer is unclear at this point. In this study, we first measured miR-22 expression level in 30 pairs of gastric cancer and matched normal tissues, two normal and six gastric cancer cell lines by real-time quantitative RT-PCR. We found that the expression of miR-22 in gastric cancer tissues and cell lines was much lower than that in normal control, respectively. Transfection of miR-22 expression plasmid could significantly inhibit the cell migration and invasion in SGC-7901 and NCL-N87 gastric cancer cell lines. Moreover, we also showed that Sp1 was negatively regulated by miR-22 at the posttranscriptional level, via a specific target site within the 3′UTR by luciferase reporter assay. The expression of Sp1 was inversely correlated with miR-22 expression in gastric cancer tissues, and knockdown of Sp1 by siRNA inhibited cell malignant behaviors. Thus, our findings suggest that miR-22 acts as tumor suppressor by targeting the Sp1 gene and inhibiting gastric cancer cell migration and invasion. The findings of this study contribute to current understanding of the functions of miR-22 in gastric cancer.
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