title: Aryl hydrocarbon receptor signaling involved in the invasiveness of LNCaP cells.
abstract: There is now mounting evidence that the aryl hydrocarbon receptor (AhR) plays an important role in physiologic responses such as development, cell cycle regulation, immune function and also malignant transformation in various tissues. The strong nuclear AhR expression is observed in the invasive phenotype, and an elevated nuclear AhR expression is associated with a poor prognosis of human prostate cancer. On the other hand, there are conflicting results that the AhR deficiency results in increased susceptibility to prostate tumors in mouse model. In the present study, we investigated AhR expression and its role in the growth and invasiveness of human prostate cancer cells. The AhR protein expression was detected in prostate cancer cell lines and human prostate cancer tissues. A small interfering RNA targeting AhR, constitutive active AhR expression vector, and AhR agonist and antagonist were used to moderate its expression and signaling. The induction of AhR signaling attenuated invasiveness of prostate cancer cells without affecting the cellular growth rate. These results suggest that AhR signaling in prostate cancer cells facilitates invasion of these cells, and modulation with this signaling can be a potential therapeutic target of invasive tumors.
authors.affiliation: Department of Urology, Teikyo University School of Medicine, Tokyo, Japan.
authors.forename: Hisamitsu
authors.initials: H
authors.lastname: Ide
authors.affiliation: Department of Urology, Teikyo University School of Medicine, Tokyo, Japan.
authors.forename: Yan
authors.initials: Y
authors.lastname: Lu
authors.affiliation: Department of Urology, The First Affiliated Hospital of Harbin Medical University, Heilongjiang, China.
authors.forename: Jingsong
authors.initials: J
authors.lastname: Yu
authors.affiliation: Department of Urology, Teikyo University School of Medicine, Tokyo, Japan.
authors.forename: Takahiro
authors.initials: T
authors.lastname: Noguchi
authors.affiliation: Department of Urology, Juntendo University, Graduate School of Medicine, Tokyo, Japan.
authors.forename: Mayuko
authors.initials: M
authors.lastname: Kanayama
authors.affiliation: Department of Urology, Teikyo University School of Medicine, Tokyo, Japan.
authors.forename: Satoru
authors.initials: S
authors.lastname: Muto
authors.affiliation: Department of Urology, Teikyo University School of Medicine, Tokyo, Japan.
authors.forename: Raizo
authors.initials: R
authors.lastname: Yamaguchi
authors.affiliation: Department of Urology, Teikyo University School of Medicine, Tokyo, Japan.|Department of Urology, Juntendo University, Graduate School of Medicine, Tokyo, Japan.
authors.forename: Suguru
authors.initials: S
authors.lastname: Kawato
authors.affiliation: Department of Urology, Juntendo University, Graduate School of Medicine, Tokyo, Japan. shorie@juntendo.ac.jp.
authors.forename: Shigeo
authors.initials: S
authors.lastname: Horie
mesh_terms: D045744:Cell Line, Tumor; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D008297:Male; D009361:Neoplasm Invasiveness / Q000235:genetics; D011471:Prostatic Neoplasms / Q000235:genetics* / Q000473:pathology*; D018336:Receptors, Aryl Hydrocarbon / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D015398:Signal Transduction / Q000235:genetics* / Q000502:physiology*
chemical_list: D018336:Receptors, Aryl Hydrocarbon
keywords: Aryl hydrocarbon receptor; Invasion; Prostate cancer