Role of methionine adenosyltransferase 2A and S-adenosylmethionine in mitogen-induced growth of human colon cancer cells.

Role of methionine adenosyltransferase 2A and S-adenosylmethionine in mitogen-induced growth of human colon cancer cells. Research Abstract Details 

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Role of methionine adenosyltransferase 2A and S-adenosylmethionine in mitogen-induced growth of human colon cancer cells. Abstract Text:

Hui Chen,Meng Xia,Mark Lin,Heping Yang,John Kuhlenkamp,Tony Li,Nicole M Sodir,Yong-Heng Chen,Heinz Josef-Lenz,Peter W Laird,Steven Clarke, Mato,Shelly C Lu,Hui Chen,Meng Xia,Mark Lin,Heping Yang,John Kuhlenkamp,Tony Li,Nicole M Sodir,Yong-Heng Chen,Heinz Josef-Lenz,Peter W Laird,Steven Clarke, Mato,Shelly C Lu,

BACKGROUND & AIMS: Two genes (MAT1A and MAT2A) encode for methionine adenosyltransferase, an essential enzyme responsible for S-adenosylmethionine (SAMe) biosynthesis. MAT1A is expressed in liver, whereas MAT2A is widely distributed. In liver, increased MAT2A expression is associated with growth, while SAMe inhibits MAT2A expression and growth. The role of MAT2A in colon cancer in unknown. The aims of this study were to examine whether MAT2A expression and SAMe and its metabolite methylthioadenosine (MTA) can modulate growth of colon cancer cells. METHODS: Studies were conducted using resected colon cancer specimens, polyps from Min mice, and human colon cancer cell lines RKO and HT-29. MAT2A expression was measured by real-time polymerase chain reaction and cell growth by the 3-(4,5-dimethylthiazolyl-2-yl)-2,5-diphenyltetrazolium bromide assay. RESULTS: In 12 of 13 patients and all 9 polyps from Min mice, the MAT2A messenger RNA levels were 200%-340% of levels in adjacent normal tissues, respectively. Epidermal growth factor, insulin-like growth factor 1, and leptin increased growth and up-regulated MAT2A expression and MAT2A promoter activity in RKO and HT-29 cells. SAMe and MTA lowered the baseline expression of MAT2A and blocked the growth factor-mediated increase in MAT2A expression and growth in colon cancer cell lines. Importantly, the mitogenic effect of these growth factors was inhibited if MAT2A induction was prevented by RNA interference. SAMe and MTA supplementation in drinking water increased intestinal SAMe levels and lowered MAT2A expression. CONCLUSIONS: Similar to the liver, up-regulation of MAT2A also provides a growth advantage and SAMe and MTA can block mitogenic signaling in colon cancer cells.

Role of methionine adenosyltransferase 2A and S-adenosylmethionine in mitogen-induced growth of human colon cancer cells. Publishing Authors By Initials

H Chen,M Xia,M Lin,H Yang,J Kuhlenkamp,T Li,NM Sodir,YH Chen,H Josef-Lenz,PW Laird,S Clarke,JM Mato,SC Lu,H Chen,M Xia,M Lin,H Yang,J Kuhlenkamp,T Li,NM Sodir,YH Chen,H Josef-Lenz,PW Laird,S Clarke,JM Mato,SC Lu,

For similar amino acids, sulfur: methionine: s-adenosylmethionine research abstracts see: amino acids, sulfur: methionine: s-adenosylmethionine research

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Role of methionine adenosyltransferase 2A and S-adenosylmethionine in mitogen-induced growth of human colon cancer cells. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Gastroenterology

VOLUME: 133

Page Numbers: 207-18

Journal Abbreviation: Gastroenterology

ISSN: 0016-5085

DAY: 11

MONTH: 04

YEAR: 2007

Role of methionine adenosyltransferase 2A and S-adenosylmethionine in mitogen-induced growth of human colon cancer cells. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 374630

Role of methionine adenosyltransferase 2A and S-adenosylmethionine in mitogen-induced growth of human colon cancer cells. Keywords Mesh Terms:

KEYWORDS: S-Adenosylmethionine

MESH TERMS: pharmacology

Chemical & Substance for Abstract: Role of methionine adenosyltransferase 2A and S-adenosylmethionine in mitogen-induced growth of human colon cancer cells. Information

Substance Name: Methionine Adenosyltransferase

Registry Number: EC 2.5.1.6

Grant and Affiliation Information for Role of methionine adenosyltransferase 2A and S-adenosylmethionine in mitogen-induced growth of human colon cancer cells.

AFFILIATION: Division of Gastroenterology and Liver Diseases, University of Southern California Research Center for Liver Diseases, University of Southern California, Los Angeles, California 90033, USA.

Country: United States

AGENCY: United States NIDDK

GRANT: P30DK48522

ACRONYM: DK

MEDLINETA: Gastroenterology

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