ICAM-3-induced cancer cell proliferation through the PI3K/Akt pathway

Yong Geon Kim, Mi Jin Kim, Jong Seok Lim, Myeong Sok Lee, Jun Suk Kim, Young Do Yoo

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

ICAM-3 interacts with LFA1, and is involved in the intercellular adhesion of leukocytes as well as in the mainenance of cell survival. It has also been suggested to induce cancer cell proliferation but the precise signaling pathway is unclear. The aim of this study was to determine the ICAM-3-activated downstream pathway in H1299 lung cancer cells. The level of ICAM-3-induced cell growth was examined using BrdU incorporation, which is a colony-forming assay, FACS analysis, and cell counting. The results showed that ICAM-3 expression induces cancer cell proliferation. In addition, FAK, Akt, PDK1, GSK-3β, BAD, and PTEN were phosphorylated by ICAM-3-overexpression, resulting in enhanced cell proliferation. In conclusion, ICAM-3 expression induces cancer cell proliferation, and an increase in ICAM-3 expression can contribute to cancer progression.

Original languageEnglish
Pages (from-to)103-110
Number of pages8
JournalCancer Letters
Volume239
Issue number1
DOIs
Publication statusPublished - 2006 Jul 28

Fingerprint

Cell proliferation
Phosphatidylinositol 3-Kinases
Cell Proliferation
Neoplasms
Cells
Glycogen Synthase Kinase 3
Cell growth
Bromodeoxyuridine
Assays
Lung Neoplasms
Cell Survival
Leukocytes
Adhesion
Growth

Keywords

  • Human lung cancer
  • ICAM-3
  • MAPK
  • PI3K/Akt
  • Proliferation

ASJC Scopus subject areas

  • Cancer Research
  • Molecular Biology
  • Oncology

Cite this

ICAM-3-induced cancer cell proliferation through the PI3K/Akt pathway. / Kim, Yong Geon; Kim, Mi Jin; Lim, Jong Seok; Lee, Myeong Sok; Kim, Jun Suk; Yoo, Young Do.

In: Cancer Letters, Vol. 239, No. 1, 28.07.2006, p. 103-110.

Research output: Contribution to journalArticle

Kim, Yong Geon ; Kim, Mi Jin ; Lim, Jong Seok ; Lee, Myeong Sok ; Kim, Jun Suk ; Yoo, Young Do. / ICAM-3-induced cancer cell proliferation through the PI3K/Akt pathway. In: Cancer Letters. 2006 ; Vol. 239, No. 1. pp. 103-110.
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