title: Silencing of CXCR4 blocks progression of ovarian cancer and depresses canonical Wnt signaling pathway.
abstract: OBJECTIVE
  CXC chemokine receptor 4 (CXCR4) was considered to be an important factor in cancer cell metastasis. This study was aimed to examine the expression of CXCR4 in ovarian cancer and determine the functions and the possible mechanisms of CXCR4 in the progression of ovarian cancer.
  
  
  METHODS
  CXC chemokine receptor 4 messenger RNA expression in normal ovarian tissues, malignant epithelial ovarian tumors, and 3 ovarian cancer cell lines was analyzed. Immunohistochemical analysis was used to detect the protein expression of CXCR4 and β-catenin in normal and malignant ovarian tissues. The effect of CXCR4 inhibition on cell proliferation and invasion was determined.
  
  
  RESULTS
  CXC chemokine receptor 4 was highly expressed in malignant ovarian tumors and ovarian cancer cell lines, and the different expression of CXCR4 was observed between the ovarian cancers with lymph node metastasis and without lymph node metastasis. Furthermore, The CXCR4 expression was correlated with β-catenin expression in ovarian tissues. Moreover, knockdown of CXCR4 could obviously reduce proliferation and invasion of ovarian cancer cell and inhibit Wnt target genes and mesenchymal markers such as vimentin and SLUG expression.
  
  
  CONCLUSIONS
  CXC chemokine receptor 4 plays a critical role in the metastasis of human ovarian cancer possibly through modulating the Wnt/β-catenin pathway. CXC chemokine receptor 4 is a potential therapeutic target for treatment of ovarian cancer.
authors: Department of Obstetrics and Gynecology, Huazhong University of Science and Technology, Wuhan, China.
authors: Jia
authors: J
authors: Wang
authors: Jing
authors: J
authors: Cai
authors: Fang
authors: F
authors: Han
authors: Chun
authors: C
authors: Yang
authors: Qiaoling
authors: Q
authors: Tong
authors: Ting
authors: T
authors: Cao
authors: Liying
authors: L
authors: Wu
authors: Zehua
authors: Z
authors: Wang
mesh_terms: D018262:Adenocarcinoma, Clear Cell / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D000293:Adolescent; D000328:Adult; D000368:Aged; D018269:Carcinoma, Endometrioid / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D045744:Cell Line, Tumor; D018282:Cystadenocarcinoma, Mucinous / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D018284:Cystadenocarcinoma, Serous / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D020868:Gene Silencing; D006801:Humans; D008207:Lymphatic Metastasis; D008875:Middle Aged; D009362:Neoplasm Metastasis; D010051:Ovarian Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000378:metabolism; D019718:Receptors, CXCR4 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D060449:Wnt Signaling Pathway / Q000502:physiology*; D055815:Young Adult; D051176:beta Catenin / Q000378:metabolism*
chemical_list: C527276:CXCR4 protein, human; D012333:RNA, Messenger; D019718:Receptors, CXCR4; D051176:beta Catenin