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

doi:10.1016/j.canlet.2005.07.023

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

Department of Biomedical Sciences

Research output: Contribution to journal › Article › peer-review

12 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 language	English
Pages (from-to)	103-110
Number of pages	8
Journal	Cancer letters
Volume	239
Issue number	1
DOIs	https://doi.org/10.1016/j.canlet.2005.07.023
Publication status	Published - 2006 Jul 28

Keywords

Human lung cancer
ICAM-3
MAPK
PI3K/Akt
Proliferation

ASJC Scopus subject areas

Oncology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.canlet.2005.07.023

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title = "ICAM-3-induced cancer cell proliferation through the PI3K/Akt pathway",

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.",

keywords = "Human lung cancer, ICAM-3, MAPK, PI3K/Akt, Proliferation",

author = "Kim, {Yong Geon} and Kim, {Mi Jin} and Lim, {Jong Seok} and Lee, {Myeong Sok} and Kim, {Jun Suk} and Yoo, {Young Do}",

note = "Funding Information: This research was supported by a grant of the Korea Research Foundation Grant; Grant number: KRF-2002-E00066 and by a grant from the Molecular and Cellular BioDiscovery Research Program (M1-0311-00-0035) of the Ministry of Science and Technology of Korea. Work at Sookmyung Women's University was supported by a grant (R11-2005-017-00000-0) of the Research Center for Woman's Diseases of the KOSEF. ",

year = "2006",

month = jul,

day = "28",

doi = "10.1016/j.canlet.2005.07.023",

language = "English",

volume = "239",

pages = "103--110",

journal = "Cancer Letters",

issn = "0304-3835",

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TY - JOUR

T1 - ICAM-3-induced cancer cell proliferation through the PI3K/Akt pathway

AU - Kim, Yong Geon

AU - Kim, Mi Jin

AU - Lim, Jong Seok

AU - Lee, Myeong Sok

AU - Kim, Jun Suk

AU - Yoo, Young Do

N1 - Funding Information: This research was supported by a grant of the Korea Research Foundation Grant; Grant number: KRF-2002-E00066 and by a grant from the Molecular and Cellular BioDiscovery Research Program (M1-0311-00-0035) of the Ministry of Science and Technology of Korea. Work at Sookmyung Women's University was supported by a grant (R11-2005-017-00000-0) of the Research Center for Woman's Diseases of the KOSEF.

PY - 2006/7/28

Y1 - 2006/7/28

N2 - 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.

AB - 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.

KW - Human lung cancer

KW - ICAM-3

KW - MAPK

KW - PI3K/Akt

KW - Proliferation

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M3 - Article

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AN - SCOPUS:33745344607

SN - 0304-3835

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SP - 103

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JO - Cancer Letters

JF - Cancer Letters

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ER -

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

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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