Claudin-1 is associated with invasive growth of human pancreatic cancer cells

  • Kondo Jun
    Department of Pathology and Bioscience, Hirosaki University Graduate School of Medicine
  • Sato Fuyuki
    Department of Pathology and Bioscience, Hirosaki University Graduate School of Medicine
  • Wu Yunyan
    Department of Pathology and Bioscience, Hirosaki University Graduate School of Medicine
  • Seino Hiroko
    Department of Pathology and Bioscience, Hirosaki University Graduate School of Medicine
  • Morohashi Satoko
    Department of Pathology and Bioscience, Hirosaki University Graduate School of Medicine
  • Kijima Hiroshi
    Department of Pathology and Bioscience, Hirosaki University Graduate School of Medicine

Bibliographic Information

Other Title
  • ヒト膵癌細胞における claudin-1 発現と浸潤性増殖の関連

Search this article

Abstract

    Claudin is one of tight junction proteins which connect with the actin cytoskeleton and participate in the intracellular signaling. However, the significance of claudin in pancreatic cancer is understood not yet extensively. We examined the relationship between claudin-1 and invasion in PANC-1 and MIA PaCa-2 human pancreatic cancer cells, and investigated the functions of claudin-1 in invasive growth of pancreatic cancer cells. Claudin-1 knockdown by siRNA (claudin siRNA) affected the subcellular localization in the pancreatic cancer cells, and claudin-1 siRNA increased numbers of invasive pancreatic cancer PANC-1 and MIA PaCa-2 cells. Claudin-1 siRNA did not significantly affect expression levels of β-catenin, E-cadherin, α-smooth muscle actin, Bcl-2, and Bax in PANC-1 and MIA PaCa-2 cells. In addition, claudin-1 siRNA showed no significant change in the cell proliferation. We concluded that claudin-1 is significantly associated with invasive growth of human pancreatic cancer cells.

Journal

  • Hirosaki Medical Journal

    Hirosaki Medical Journal 63 (2-4), 127-135, 2012

    Hirosaki University Graduate School of Medicine,Hirosaki Medical Society

Details 詳細情報について

Report a problem

Back to top