title: KCC1 gene advances cell invasion ability by regulating ERK signaling pathway in endometrial cancer HEC-1B cell line.
abstract: BACKGROUND
  Human potassium chloride cotransporter-1 (KCC1) gene is expressed in endometrial cancer and related to metastasis of endometrial cancer. However, whether KCC1 contributes to invasion and metastasis of endometrial cancer has not been thoroughly investigated. The purpose of this study is to research the alternation effect of insulin-like growth factor I (IGF-I) on the expression of KCC1 in endometrial cancer HEC-1B cells and to explore the mechanism of how KCC1 regulates the invasion ability of HEC-1B cells through the extracellular signal-regulated kinase (ERK) signaling pathway.
  
  
  METHODS
  First, the inhibitive effect of RNA interference to KCC1 was detected by semiquantitative reverse transcriptase-polymerase chain reaction. Western blot was used to measure expression changes of KCC1 after exposure to IGF-I in the HEC-1B cells. The change in quantity of phosphorylated ERK1/2 (p-ERK1/2) and cell invasion ability also were measured. After RNA interference and treatment with U0126, the quantity of p-ERK1/2 and the cell invasion ability were measured again.
  
  
  RESULTS
  After the application of IGF-I on the HEC-1B cells, the expression of KCC1 and p-ERK1/2 increased dramatically, and the cell invasion ability advanced. RNA interference could inhibit the expression of KCC1, and the quantity of p-ERK1/2 and the cell invasion ability decreased even under the effect of IGF-I. Furthermore, after treatment with U0126, the cell invasion ability no longer advanced even under the effect of IGF-I either.
  
  
  CONCLUSIONS
  Insulin-like growth factors I can induce the upregulation of KCC1 gene, and KCC1 gene participates in the invasion ability of HEC-1B cells through the ERK signaling pathway.
authors.affiliation: Department of Neurobiology, China Medical University, and Department of Gynaecology and Obstetrics, The Affiliated Shengjing Hospital, Shenyang, People's Republic of China.
authors.forename: Chao
authors.initials: C
authors.lastname: Shang
authors.forename: Yan-ming
authors.initials: YM
authors.lastname: Lu
authors.forename: Li-rong
authors.initials: LR
authors.lastname: Meng
mesh_terms: D002070:Butadienes / Q000494:pharmacology; D002277:Carcinoma / Q000235:genetics* / Q000473:pathology; D002448:Cell Adhesion / Q000187:drug effects / Q000235:genetics; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects / Q000235:genetics*; D004353:Drug Evaluation, Preclinical; D016889:Endometrial Neoplasms / Q000235:genetics* / Q000473:pathology; D005260:Female; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology; D048369:MAP Kinase Kinase 1 / Q000037:antagonists & inhibitors; D020935:MAP Kinase Signaling System / Q000187:drug effects / Q000235:genetics* / Q000502:physiology; D009361:Neoplasm Invasiveness; D009570:Nitriles / Q000494:pharmacology; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D027981:Symporters / Q000235:genetics*; D015854:Up-Regulation / Q000187:drug effects / Q000235:genetics; D000096922:K Cl- Cotransporters
chemical_list: D002070:Butadienes; D007334:Insulin-Like Growth Factor I; D048369:MAP Kinase Kinase 1; D009570:Nitriles; D047428:Protein Kinase Inhibitors; D027981:Symporters; D000096922:K Cl- Cotransporters; C113580:U 0126; C482125:MAP2K1 protein, human