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Loss of tricellular tight junction protein LSR promotes cell invasion and migration via upregulation of TEAD1/AREG in human endometrial cancer.
Shimada, Hiroshi; Abe, Shyuetsu; Kohno, Takayuki; Satohisa, Seiro; Konno, Takumi; Takahashi, Syunta; Hatakeyama, Tsubasa; Arimoto, Chihiro; Kakuki, Takuya; Kaneko, Yakuto; Takano, Ken-Ichi; Saito, Tsuyoshi; Kojima, Takashi.
Afiliação
  • Shimada H; Departments of Obstetrics and Gynecology, University School of Medicine, Sapporo, Japan.
  • Abe S; Department of Cell Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Kohno T; Departments of Obstetrics and Gynecology, University School of Medicine, Sapporo, Japan.
  • Satohisa S; Department of Cell Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Konno T; Department of Cell Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Takahashi S; Departments of Obstetrics and Gynecology, University School of Medicine, Sapporo, Japan.
  • Hatakeyama T; Department of Cell Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Arimoto C; Department of Cell Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Kakuki T; Department of Cell Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Kaneko Y; Department of Cell Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Takano KI; Department of Cell Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Saito T; Departments of Otolaryngology, Sapporo Medical, University School of Medicine, Sapporo, Japan.
  • Kojima T; Department of Cell Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Sci Rep ; 7: 37049, 2017 01 10.
Article em En | MEDLINE | ID: mdl-28071680
ABSTRACT
Lipolysis-stimulated lipoprotein receptor (LSR) is a unique molecule of tricellular contacts of normal and cancer cells. We investigated how the loss of LSR induced cell migration, invasion and proliferation in endometrial cancer cell line Sawano. mRNAs of amphiregulin (AREG) and TEA domain family member 1 (TEAD1) were markedly upregulated by siRNA-LSR. In endometrial cancer tissues, downregulation of LSR and upregulation of AREG were observed together with malignancy, and Yes-associated protein (YAP) was present in the nuclei. siRNA-AREG prevented the cell migration and invasion induced by siRNA-LSR, whereas treatment with AREG induced cell migration and invasion. LSR was colocalized with TRIC, angiomotin (AMOT), Merlin and phosphorylated YAP (pYAP). siRNA-LSR increased expression of pYAP and decreased that of AMOT and Merlin. siRNA-YAP prevented expression of the mRNAs of AREG and TEAD1, and the cell migration and invasion induced by siRNA-LSR. Treatment with dobutamine and 2-deoxy-D-glucose and glucose starvation induced the pYAP expression and prevented the cell migration and invasion induced by siRNA-LSR. siRNA-AMOT decreased the Merlin expression and prevented the cell migration and invasion induced by siRNA-LSR. The loss of LSR promoted cell invasion and migration via upregulation of TEAD1/AREG dependent on YAP/pYAP and AMOT/Merlin in human endometrial cancer cells.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Neoplasias do Endométrio / Receptores de Lipoproteínas / Junções Íntimas / Células Epiteliais Limite: Female / Humans Idioma: En Revista: Sci Rep Ano de publicação: 2017 Tipo de documento: Article País de afiliação: Japão

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Neoplasias do Endométrio / Receptores de Lipoproteínas / Junções Íntimas / Células Epiteliais Limite: Female / Humans Idioma: En Revista: Sci Rep Ano de publicação: 2017 Tipo de documento: Article País de afiliação: Japão