miR-212 promotes pancreatic cancer cell growth and invasion by targeting the hedgehog signaling pathway receptor patched-1

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• 作者：Chenchao Ma (7)
  Kate Nong (7)
  Bo Wu (7)
  Bo Dong (7)
  Yueqing Bai (8)
  Hongda Zhu (7)
  Weiwei Wang (7)
  Xinyu Huang (7)
  Zhou Yuan (7)
  Kaixing Ai (7)
  
  7. Department of General Surgery ; The Sixth People鈥檚 Hospital Affiliated to Shanghai Jiaotong University ; Shanghai ; 200233 ; China
  8. Department of Pathology ; The Sixth People鈥檚 Hospital Affiliated to Shanghai Jiaotong University ; Shanghai ; 200233 ; China
  
• 关键词：miR ; 212 ; Patched ; 1 ; Pancreatic cancer ; Proliferation ; Migration ; Invasion
• 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：1,474 KB
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• 刊物主题：Oncology; Cancer Research;
• 出版者：BioMed Central
• ISSN：1756-9966

文摘

Background microRNAs (miRNAs) are a class of small non-coding RNAs that play important roles in carcinogenesis. In the present study, we investigated the effect of miR-212 on pancreatic ductal adenocarcinoma (PDAC) and its target protein. Methods Quantitative real-time PCR(qRT-PCR) was performed to detect the expression of miR-212 in PDAC tissues and pancreatic cancer cell lines. miR-212 mimic, miR-212 inhibitor and negative control were transfected into pancreatic cancer cells and the effect of miR-212 up-regulation and down-regulation on the proliferation, migration and invasion of cells were investigated. Furthermore, the mRNA and protein levels of Patched-1(PTCH1) were measured. Meanwhile, luciferase assays were performed to validate PTCH1 as miR-212 target in PDAC. Results miR-212 was up-regulated in PDAC tissues and cells.Using both gain-of function and loss-of function experiments, a pro-oncogenic function of miR-212 was demonstrated in PDAC. Moreover, up-regulated of PTCH1 could attenuate the effect induced by miR-212. Conclusion These data suggest that miR-212 could facilitate PDAC progression and metastasis through targeting PTCH1, implicating a novel mechanism for the progression of PDAC.