title: Substance P Promotes the Progression of Endometrial Adenocarcinoma.
abstract: It has been demonstrated that substance P (SP) promotes while neurokinin-1 receptor (NK-1R) antagonist inhibits the proliferation of several human cancer cells. Currently, it is still unknown whether such actions exist in human endometrial carcinoma. This study aimed to explore the role of SP/NK-1R signaling in the progression of endometrial adenocarcinoma.
  
  
  
  The expression levels of SP and NK-1R in endometrial adenocarcinoma tissues and Ishikawa cell line were detected by real-time quantitative PCR and Western blot analysis. The effects of SP on Ishikawa cells proliferation and invasion were analyzed using MTT assay and transwell matrigel invasion assay, respectively. The expression levels of matrix metalloproteinase 9 (MMP-9) and vascular endothelial growth factor C (VEGF-C) in Ishikawa cells after administration of SP were detected by real-time quantitative RCR and Western blot analysis.
  
  
  
  The expression levels of SP and NK-1R were significantly higher in endometrial adenocarcinoma tissues and Ishikawa cells than in normal endometrium. Substance P significantly enhanced the proliferation and invasion of Ishikawa cells. In addition, SP induced the expression of MMP-9 and VEGF-C in Ishikawa cells, whereas NK-1R antagonist inhibited these effects.
  
  
  
  Substance P plays an important role in the development of endometrial carcinoma by inducing the expression of MMP-9 and VEGF-C and promoting cancer cell proliferation and metastasis, which can be blocked by NK-1R antagonist.
authors.affiliation: *Department of Gynecology, The Fourth Hospital, Hebei Medical University; †Department of Surgery, Hospital of Hebei Province Crop of Chinese Armed Police Force; and ‡Department of Traditional Chinese Medicine, The Fourth Hospital, Hebei Medical University, Shijiazhuang, Hebei, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Ma
authors.forename: Shifa
authors.initials: S
authors.lastname: Yuan
authors.forename: Jianxin
authors.initials: J
authors.lastname: Cheng
authors.forename: Shan
authors.initials: S
authors.lastname: Kang
authors.forename: Wenhong
authors.initials: W
authors.lastname: Zhao
authors.forename: Jie
authors.initials: J
authors.lastname: Zhang
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism* / Q000473:pathology; D045744:Cell Line, Tumor; D018450:Disease Progression; D016889:Endometrial Neoplasms / Q000378:metabolism* / Q000473:pathology; D004790:Enzyme Induction / Q000187:drug effects; D005260:Female; D006801:Humans; D020780:Matrix Metalloproteinase 9 / Q000096:biosynthesis; D008875:Middle Aged; D018040:Receptors, Neurokinin-1 / Q000096:biosynthesis / Q000378:metabolism; D015398:Signal Transduction; D013373:Substance P / Q000096:biosynthesis / Q000378:metabolism* / Q000494:pharmacology; D042582:Vascular Endothelial Growth Factor C / Q000096:biosynthesis
chemical_list: D018040:Receptors, Neurokinin-1; C467486:VEGFC protein, human; D042582:Vascular Endothelial Growth Factor C; D013373:Substance P; C579270:MMP9 protein, human; D020780:Matrix Metalloproteinase 9