title: MiR-21 regulates biological behavior through the PTEN/PI-3 K/Akt signaling             pathway in human colorectal cancer cells.
abstract: The aim of this study was to determine a role of microRNA-21 (miR-21) in             colorectal cancer (CRC) and to elucidate the regulation of phosphatase and tensin             homologue (PTEN) gene by miR-21. MiR-21 expression was investigated in 30 CRC             samples and five CRC cell lines. In this study, we show that the expression of             miR-21 was overexpressed in CRC compared with adenomas and normal tissues. Patients             with poor differentiation, lymph node metastasis and advanced TNM stage showed             significantly high expression of miR-21. Inhibition of miR-21 in the HCT116 cell             line reduced cellular proliferation, migration and invasion, induced apoptosis             and inhibited cell cycle progression. The PTEN protein levels in CRC tissues and             cells had an inverse correlation with miR-21 expression. Anti-miR-21-transfected             cells increased PTEN protein expression without changing the PTEN mRNA level and             increased a luciferase-reporter activity. MiR-21 targets PTEN at the post-transcriptional             level and regulates cell proliferation and invasion in CRC. It may serve as a             novel therapeutic target in CRC.
authors.affiliation: Department of General Surgery, First Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China. 280343115@qq.com
authors.forename: Binghong
authors.initials: B
authors.lastname: Xiong
authors.forename: Yong
authors.initials: Y
authors.lastname: Cheng
authors.forename: Li
authors.initials: L
authors.lastname: Ma
authors.forename: Caiquan
authors.initials: C
authors.lastname: Zhang
mesh_terms: D000236:Adenoma / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D017209:Apoptosis; D015153:Blotting, Western; D002454:Cell Differentiation; D002465:Cell Movement; D049109:Cell Proliferation; D003106:Colon / Q000378:metabolism; D015179:Colorectal Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007124:Immunoenzyme Techniques; D008156:Luciferases / Q000378:metabolism; D008207:Lymphatic Metastasis; D035683:MicroRNAs / Q000037:antagonists & inhibitors / Q000235:genetics*; D009361:Neoplasm Invasiveness; D009367:Neoplasm Staging; D016376:Oligonucleotides, Antisense / Q000494:pharmacology; D051059:PTEN Phosphohydrolase / Q000235:genetics / Q000378:metabolism*; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D012007:Rectum / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction; D014407:Tumor Cells, Cultured; D014945:Wound Healing
chemical_list: C524940:MIRN21 microRNA, human; D035683:MicroRNAs; D016376:Oligonucleotides, Antisense; D012333:RNA, Messenger; D008156:Luciferases; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human