title: MiR-221 Promotes Capan-2 Pancreatic Ductal Adenocarcinoma Cells Proliferation by Targeting PTEN-Akt.
abstract: OBJECTIVE
  MicroRNAs (miRNAs, miRs) have emerged as critical regulators of cancer cell proliferation. The effect of miR-221 on cancer cell growth could be significantly changeable in different cell lines. Although miR-221 was reported to promote the cell growth of pancreatic ductal adenocarcinoma (PDAC) cells, its role in Capan-2 cell line is largely unknown.
  
  
  METHODS
  Capan-2 cells were transfected with miR-221 mimics, inhibitors, or negative controls. Cell Counting Kit-8 was used to determine cell viability. EdU staining and cell cycle analysis were used to measure cell proliferation. Western blotting was used to detect the expression levels of PTEN and phospho-Akt. The PI3K-Akt pathway activator SC-79 and inhibitor LY294002 were used to perform the rescue experiment in determining cell proliferation.
  
  
  RESULTS
  Overexpressing miR-221 significantly increased cell vitality and promoted cell proliferation and G1-to-S phase transition of the cell cycle in Capan-2 cells, while inhibition of miR-221 decreased that. The protein level of PTEN in Capan-2 cells was downregulated by overexpressing miR-221, while upregulated by inhibiting miR-221. Consistently, enhanced phosphorylation of AktSer473 was observed in miR-221 overexpressed Capan-2 cells, and the opposite result was found in miR-221 inhibited cells. LY294002 restored the pro-proliferation effect of miR-221 on Capan-2 cells, while SC-79 had no additional effect on cell proliferation in Capan-2 cells transfected with miR-221 mimics.
  
  
  CONCLUSIONS
  Our study indicates that miR-221 is an oncogenic miRNA which promotes Capan-2 cells proliferation by targeting PTEN-Akt pathway.
authors.forename: Wenzhuo
authors.initials: W
authors.lastname: Yang
authors.forename: Yanning
authors.initials: Y
authors.lastname: Yang
authors.forename: Lu
authors.initials: L
authors.lastname: Xia
authors.forename: Yuefeng
authors.initials: Y
authors.lastname: Yang
authors.forename: Fei
authors.initials: F
authors.lastname: Wang
authors.forename: Meiyi
authors.initials: M
authors.lastname: Song
authors.forename: Xiaoyu
authors.initials: X
authors.lastname: Chen
authors.forename: Jingqi
authors.initials: J
authors.lastname: Liu
authors.forename: Yang
authors.initials: Y
authors.lastname: Song
authors.forename: Yingying
authors.initials: Y
authors.lastname: Zhao
authors.forename: Changqing
authors.initials: C
authors.lastname: Yang
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D021441:Carcinoma, Pancreatic Ductal / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D035683:MicroRNAs / Q000235:genetics* / Q000378:metabolism; D051059:PTEN Phosphohydrolase / Q000032:analysis / Q000378:metabolism*; D010183:Pancreatic Ducts / Q000378:metabolism / Q000473:pathology*; D051057:Proto-Oncogene Proteins c-akt / Q000032:analysis / Q000378:metabolism*; D015398:Signal Transduction; D015854:Up-Regulation
chemical_list: D035683:MicroRNAs; D051059:PTEN Phosphohydrolase; D051057:Proto-Oncogene Proteins c-akt; C525709:MIR221, human; C494929:PTEN protein, human