RAGE activation by S100P in colon cancer stimulates growth, migration, and cell signaling pathways

Maren K. Fuentes; Shraddha S. Nigavekar; Thiruvengadam Arumugam; Craig D. Logsdon; Ann Marie Schmidt; Juliet C. Park; Emina H. Huang

doi:10.1007/s10350-006-0850-5

RAGE activation by S100P in colon cancer stimulates growth, migration, and cell signaling pathways

Maren K. Fuentes, Shraddha S. Nigavekar, Thiruvengadam Arumugam, Craig D. Logsdon, Ann Marie Schmidt, Juliet C. Park, Emina H. Huang

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

140 Scopus citations

Abstract

PURPOSE: Colon cancer is the third most prevalent cancer in the United States. However, the molecular mechanisms involved in the development and progression of colon cancer are incompletely understood. This study was initiated to explore the potential role of the receptor for advanced glycation end-products and S100P in modulation of key properties of human colon cancer cells. METHODS: Western blot, reverse transcription-polymerase chain reaction, and quantitative polymerase chain reaction were performed for detection of the receptor for advanced glycation end-products and S100P in colon cancer and matched normal colon. The influence of exogenously added S100P was analyzed on SW480 colon cancer cell line proliferation, migration, phosphorylation of mitogen activated protein kinases, and NFκB activation. To identify the mechanisms involved in these responses, coimmunoprecipitation examining the S100P/Receptor for advanced glycation end-products interaction and the effects of receptor for advanced glycation end-products inhibition in this interaction were analyzed. RESULTS: Although the receptor for advanced glycation end-products was present in normal and malignant colon specimens, only the malignant specimens expressed S100P. Treatment of SW480 cells with S100P increased proliferation and cell migration. Addition of exogenous S100P stimulated both ERK1/2 phosphorylation and NFκB activity. The interaction between S100P and the receptor for advanced glycation end-products was demonstrated by coimmunoprecipitation of these molecules from SW480 cells. Antagonism of the receptor for advanced glycation end-products blocked this interaction and the biologic effects of S100P on these cells. CONCLUSIONS: These data indicate that S100P is expressed at greater levels in colon cancer than matched normal tissue and that S100P stimulates colon cancer cell growth, migration, Erk phosphorylation, and NFκB activation in vitro, suggesting that this ligand/receptor pair may be targeted for the development of new therapies.

Original language	English (US)
Pages (from-to)	1230-1240
Number of pages	11
Journal	Diseases of the Colon and Rectum
Volume	50
Issue number	8
DOIs	https://doi.org/10.1007/s10350-006-0850-5
State	Published - Aug 2007
Externally published	Yes

Keywords

Colon cancer
MAP kinase
Migration
NFκB
Proliferation
Receptor for advanced glycation end-products
S100P

ASJC Scopus subject areas

Gastroenterology

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10.1007/s10350-006-0850-5

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@article{872218ad16d74a589cd2c84db05c7a55,

title = "RAGE activation by S100P in colon cancer stimulates growth, migration, and cell signaling pathways",

abstract = "PURPOSE: Colon cancer is the third most prevalent cancer in the United States. However, the molecular mechanisms involved in the development and progression of colon cancer are incompletely understood. This study was initiated to explore the potential role of the receptor for advanced glycation end-products and S100P in modulation of key properties of human colon cancer cells. METHODS: Western blot, reverse transcription-polymerase chain reaction, and quantitative polymerase chain reaction were performed for detection of the receptor for advanced glycation end-products and S100P in colon cancer and matched normal colon. The influence of exogenously added S100P was analyzed on SW480 colon cancer cell line proliferation, migration, phosphorylation of mitogen activated protein kinases, and NFκB activation. To identify the mechanisms involved in these responses, coimmunoprecipitation examining the S100P/Receptor for advanced glycation end-products interaction and the effects of receptor for advanced glycation end-products inhibition in this interaction were analyzed. RESULTS: Although the receptor for advanced glycation end-products was present in normal and malignant colon specimens, only the malignant specimens expressed S100P. Treatment of SW480 cells with S100P increased proliferation and cell migration. Addition of exogenous S100P stimulated both ERK1/2 phosphorylation and NFκB activity. The interaction between S100P and the receptor for advanced glycation end-products was demonstrated by coimmunoprecipitation of these molecules from SW480 cells. Antagonism of the receptor for advanced glycation end-products blocked this interaction and the biologic effects of S100P on these cells. CONCLUSIONS: These data indicate that S100P is expressed at greater levels in colon cancer than matched normal tissue and that S100P stimulates colon cancer cell growth, migration, Erk phosphorylation, and NFκB activation in vitro, suggesting that this ligand/receptor pair may be targeted for the development of new therapies.",

keywords = "Colon cancer, MAP kinase, Migration, NFκB, Proliferation, Receptor for advanced glycation end-products, S100P",

author = "Fuentes, {Maren K.} and Nigavekar, {Shraddha S.} and Thiruvengadam Arumugam and Logsdon, {Craig D.} and Schmidt, {Ann Marie} and Park, {Juliet C.} and Huang, {Emina H.}",

note = "Funding Information: Supported by K0891975 (EHH), Lockton Endowment (CDL), and CA87677 (AMS).",

year = "2007",

month = aug,

doi = "10.1007/s10350-006-0850-5",

language = "English (US)",

volume = "50",

pages = "1230--1240",

journal = "Diseases of the Colon and Rectum",

issn = "0012-3706",

publisher = "Lippincott Williams and Wilkins",

number = "8",

}

TY - JOUR

T1 - RAGE activation by S100P in colon cancer stimulates growth, migration, and cell signaling pathways

AU - Fuentes, Maren K.

AU - Nigavekar, Shraddha S.

AU - Arumugam, Thiruvengadam

AU - Logsdon, Craig D.

AU - Schmidt, Ann Marie

AU - Park, Juliet C.

AU - Huang, Emina H.

N1 - Funding Information: Supported by K0891975 (EHH), Lockton Endowment (CDL), and CA87677 (AMS).

PY - 2007/8

Y1 - 2007/8

N2 - PURPOSE: Colon cancer is the third most prevalent cancer in the United States. However, the molecular mechanisms involved in the development and progression of colon cancer are incompletely understood. This study was initiated to explore the potential role of the receptor for advanced glycation end-products and S100P in modulation of key properties of human colon cancer cells. METHODS: Western blot, reverse transcription-polymerase chain reaction, and quantitative polymerase chain reaction were performed for detection of the receptor for advanced glycation end-products and S100P in colon cancer and matched normal colon. The influence of exogenously added S100P was analyzed on SW480 colon cancer cell line proliferation, migration, phosphorylation of mitogen activated protein kinases, and NFκB activation. To identify the mechanisms involved in these responses, coimmunoprecipitation examining the S100P/Receptor for advanced glycation end-products interaction and the effects of receptor for advanced glycation end-products inhibition in this interaction were analyzed. RESULTS: Although the receptor for advanced glycation end-products was present in normal and malignant colon specimens, only the malignant specimens expressed S100P. Treatment of SW480 cells with S100P increased proliferation and cell migration. Addition of exogenous S100P stimulated both ERK1/2 phosphorylation and NFκB activity. The interaction between S100P and the receptor for advanced glycation end-products was demonstrated by coimmunoprecipitation of these molecules from SW480 cells. Antagonism of the receptor for advanced glycation end-products blocked this interaction and the biologic effects of S100P on these cells. CONCLUSIONS: These data indicate that S100P is expressed at greater levels in colon cancer than matched normal tissue and that S100P stimulates colon cancer cell growth, migration, Erk phosphorylation, and NFκB activation in vitro, suggesting that this ligand/receptor pair may be targeted for the development of new therapies.

AB - PURPOSE: Colon cancer is the third most prevalent cancer in the United States. However, the molecular mechanisms involved in the development and progression of colon cancer are incompletely understood. This study was initiated to explore the potential role of the receptor for advanced glycation end-products and S100P in modulation of key properties of human colon cancer cells. METHODS: Western blot, reverse transcription-polymerase chain reaction, and quantitative polymerase chain reaction were performed for detection of the receptor for advanced glycation end-products and S100P in colon cancer and matched normal colon. The influence of exogenously added S100P was analyzed on SW480 colon cancer cell line proliferation, migration, phosphorylation of mitogen activated protein kinases, and NFκB activation. To identify the mechanisms involved in these responses, coimmunoprecipitation examining the S100P/Receptor for advanced glycation end-products interaction and the effects of receptor for advanced glycation end-products inhibition in this interaction were analyzed. RESULTS: Although the receptor for advanced glycation end-products was present in normal and malignant colon specimens, only the malignant specimens expressed S100P. Treatment of SW480 cells with S100P increased proliferation and cell migration. Addition of exogenous S100P stimulated both ERK1/2 phosphorylation and NFκB activity. The interaction between S100P and the receptor for advanced glycation end-products was demonstrated by coimmunoprecipitation of these molecules from SW480 cells. Antagonism of the receptor for advanced glycation end-products blocked this interaction and the biologic effects of S100P on these cells. CONCLUSIONS: These data indicate that S100P is expressed at greater levels in colon cancer than matched normal tissue and that S100P stimulates colon cancer cell growth, migration, Erk phosphorylation, and NFκB activation in vitro, suggesting that this ligand/receptor pair may be targeted for the development of new therapies.

KW - Colon cancer

KW - MAP kinase

KW - Migration

KW - NFκB

KW - Proliferation

KW - Receptor for advanced glycation end-products

KW - S100P

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U2 - 10.1007/s10350-006-0850-5

DO - 10.1007/s10350-006-0850-5

M3 - Article

C2 - 17587138

AN - SCOPUS:34447623162

SN - 0012-3706

VL - 50

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EP - 1240

JO - Diseases of the Colon and Rectum

JF - Diseases of the Colon and Rectum

IS - 8

ER -

RAGE activation by S100P in colon cancer stimulates growth, migration, and cell signaling pathways

Abstract

Keywords

ASJC Scopus subject areas

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