The role of microRNA-133b and its target gene FSCN1 in gastric cancer

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• 作者：Lihua Guo (1) (2)
  Hua Bai (3)
  Dongling Zou (4)
  Tao Hong (2)
  Jie Liu (1)
  Jiaqiang Huang (2)
  Pengfei He (5)
  Qi Zhou (4)
  Jinsheng He (2)
  
  1. School of Computer and Information Technology ; Shangyuan Residence ; Haidian District ; Beijing ; 100044 ; China
  2. College of Life Sciences and Bioengineering ; Beijing Jiaotong University ; Shangyuan Residence ; Haidian District ; Beijing ; 100044 ; China
  3. Department of Ophthalmology ; General Hospital of Bei Jing Command of PLA ; #5 Nanmencang ; DongCheng District ; Beijing ; 100700 ; China
  4. Department of Gynecologic Oncology ; Chongqing Cancer Institute ; Chongqing ; 400030 ; China
  5. National Institutes for Food and Drug Control ; No.2 Tiantan Xi Li ; Beijing ; 100050 ; China
  
• 关键词：Gastric cancer ; miR ; 133b ; FSCN1 ; Tumor suppressor
• 刊名：Journal of Experimental & Clinical Cancer Research
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：33
• 期：1
• 全文大小：2,371 KB
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• 刊物主题：Oncology; Cancer Research;
• 出版者：BioMed Central
• ISSN：1756-9966

文摘

Background Increasing evidences have documented that microRNAs (miRNAs) act as oncogenes or tumor suppressors in gastric cancer (GC). In this study, we aimed to investigate the expression of miR-133b in a large number of GC samples and elucidate its role in GC carcinogenesis and the detailed mechanism. Methods We used Taqman probe stem-loop real-time PCR to accurately measure the levels of miR-133b in 100 pairs of gastric cancer tissues and the adjacent non-neoplastic tissues. miR-133b mimics were overexpressed in GC cell lines, miR-133b inhibitors were also introduced in GES cells to investigate its role on regulating cell proliferation, cell migration and cell invasion. The target of miR-133b was identified by luciferase reporter assay and western blot. Fascin actin-bundling protein 1 (FSCN1) siRNA was used to achieve the knockdown of FSCN1 in GC cells and to investigate its role on modulating GC cell proliferation and invasion. Results miR-133b was significantly down-regulated in GC cell lines and in GC tissues compared with adjacent normal tissues. Moreover, lower-level of miR-133b was also associated with venous invasion and a more aggressive tumor phenotype. Re-introduction of miR-133b in GC cells can inhibit cell proliferation, cell migration and invasion. In contrary, knockdown of miR-133b in GES cells can promote cell proliferation and invasion. Further investigation indicated that miR-133b targeted FSCN1 in GC cells and knockdown of FSCN1 can also inhibit GC cell growth and invasion. Conclusion Our findings demonstrated that miR-133b was significantly down-regulated in GC tissues and exerted its tumor suppressor role in GC cells. The investigation of the detailed mechanism showed that miR-133b directly targeted FSCN1 which functioned as an oncogenic gene in GC cells. These results suggested that miR-133b can be developed as a new diagnostic marker or therapeutic target for GC.