title: Overexpression of HepaCAM inhibits cell viability and motility through suppressing nucleus translocation of androgen receptor and ERK signaling in prostate cancer.
abstract: BACKGROUND
  HepaCAM is suppressed in a variety of human cancers, and involved in cell adhesion, growth, migration, invasion, and survival. However, the expression and function of HepaCAM in prostate cancer are still unknown.
  
  
  METHODS
  HepaCAM expression has been detected by RT-PCR, Western blotting and immunohistochemistry staining in prostate cell lines RWPE-1, LNCap, DU145, PC3, and in 75 human prostate tissue specimens, respectively. Meanwhile, the cell proliferation ability was detected by WST-8 assay. The role of HepaCAM in prostate cancer cell migration and invasion was examined by wound healing and transwell assay. And flow cytometry was used to observe the apoptosis of prostate cancer cells. Then we detected changes of Androgen Receptor translocation and ERK signaling using immunofluorescence staining and western blot after overexpression of HepaCAM.
  
  
  RESULTS
  The HepaCAM expression was significantly down-regulated in prostate cancer tissues and undetected in prostate cancer cells. However, the low HepaCAM expression was not statistically associated with clinicopathological characteristics of prostate cancer. Overexpression of HepaCAM in prostate cancer cells decreased the cell proliferation, migration and invasion, and induced the cell apoptosis. Meanwhile, HepaCAM prevented the androgen receptor translocation from the cytoplasm to the nucleus and down-regulated the MAPK/ERK signaling.
  
  
  CONCLUSIONS
  Our results suggested that HepaCAM acted as a tumor suppressor in prostate cancer. HepaCAM inhibited cell viability and motility which might be through suppressing the nuclear translocation of Androgen Receptor and down-regulating the ERK signaling. Therefore, it was indicated that HepaCAM may be a potential therapeutic target for prostate cancer.
authors.affiliation: Key Laboratory of Diagnostics Medicine designated by the Ministry of Education, Chongqing Medical University, Chongqing, China.
authors.forename: Xuedong
authors.initials: X
authors.lastname: Song
authors.forename: Yin
authors.initials: Y
authors.lastname: Wang
authors.forename: Hongfei
authors.initials: H
authors.lastname: Du
authors.forename: Yanru
authors.initials: Y
authors.lastname: Fan
authors.forename: Xue
authors.initials: X
authors.lastname: Yang
authors.forename: Xiaorong
authors.initials: X
authors.lastname: Wang
authors.forename: Xiaohou
authors.initials: X
authors.lastname: Wu
authors.forename: Chunli
authors.initials: C
authors.lastname: Luo
mesh_terms: D021581:Active Transport, Cell Nucleus; D000328:Adult; D000368:Aged; D017209:Apoptosis; D018797:Cell Cycle Proteins; D045744:Cell Line, Tumor; D002465:Cell Movement; D002470:Cell Survival; D048049:Extracellular Signal-Regulated MAP Kinases / Q000502:physiology*; D006801:Humans; D020935:MAP Kinase Signaling System / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D009361:Neoplasm Invasiveness; D011467:Prostate / Q000737:chemistry; D011471:Prostatic Neoplasms / Q000737:chemistry / Q000473:pathology*; D021381:Protein Transport; D011506:Proteins / Q000032:analysis / Q000502:physiology*; D011944:Receptors, Androgen / Q000378:metabolism*
chemical_list: D018797:Cell Cycle Proteins; C487620:HEPACAM protein, human; D011506:Proteins; D011944:Receptors, Androgen; D048049:Extracellular Signal-Regulated MAP Kinases
keywords: Androgen Receptor; ERK signaling; HepaCAM; Prostate cancer