Peroxisome proliferator-activated receptor-δ attenuates colon carcinogenesis

Fred S. Harman; Christopher J. Nicol; Holly E. Marin; Jerrold M. Ward; Frank J. Gonzalez; Jeffrey M. Peters

doi:10.1038/nm1026

Peroxisome proliferator-activated receptor-δ attenuates colon carcinogenesis

Fred S. Harman
, Christopher J. Nicol
, Holly E. Marin
, Jerrold M. Ward
, Frank J. Gonzalez
, Jeffrey M. Peters

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

196 Scopus citations

Abstract

Peroxisome proliferator-activated receptor-δ (PPAR-δ; also known as PPAR-β) is expressed at high levels in colon tumors, but its contribution to colon cancer is unclear. We examined the role of PPAR-δ in colon carcinogenesis using PPAR-δ-deficient (Ppard^-/-) mice. In both the Min mutant and chemically induced mouse models, colon polyp formation was significantly greater in mice nullizygous for PPAR-δ. In contrast to previous reports suggesting that activation of PPAR-δ potentiates colon polyp formation, here we show that PPAR-δ attenuates colon carcinogenesis.

Original language	English (US)
Pages (from-to)	481-483
Number of pages	3
Journal	Nature Medicine
Volume	10
Issue number	5
DOIs	https://doi.org/10.1038/nm1026
State	Published - May 2004

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

SDG 3 Good Health and Well-being

All Science Journal Classification (ASJC) codes

General Biochemistry, Genetics and Molecular Biology

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10.1038/nm1026

Cite this

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title = "Peroxisome proliferator-activated receptor-δ attenuates colon carcinogenesis",

abstract = "Peroxisome proliferator-activated receptor-δ (PPAR-δ; also known as PPAR-β) is expressed at high levels in colon tumors, but its contribution to colon cancer is unclear. We examined the role of PPAR-δ in colon carcinogenesis using PPAR-δ-deficient (Ppard-/-) mice. In both the Min mutant and chemically induced mouse models, colon polyp formation was significantly greater in mice nullizygous for PPAR-δ. In contrast to previous reports suggesting that activation of PPAR-δ potentiates colon polyp formation, here we show that PPAR-δ attenuates colon carcinogenesis.",

author = "Harman, \{Fred S.\} and Nicol, \{Christopher J.\} and Marin, \{Holly E.\} and Ward, \{Jerrold M.\} and Gonzalez, \{Frank J.\} and Peters, \{Jeffrey M.\}",

year = "2004",

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doi = "10.1038/nm1026",

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pages = "481--483",

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T1 - Peroxisome proliferator-activated receptor-δ attenuates colon carcinogenesis

AU - Harman, Fred S.

AU - Nicol, Christopher J.

AU - Marin, Holly E.

AU - Ward, Jerrold M.

AU - Gonzalez, Frank J.

AU - Peters, Jeffrey M.

PY - 2004/5

Y1 - 2004/5

N2 - Peroxisome proliferator-activated receptor-δ (PPAR-δ; also known as PPAR-β) is expressed at high levels in colon tumors, but its contribution to colon cancer is unclear. We examined the role of PPAR-δ in colon carcinogenesis using PPAR-δ-deficient (Ppard-/-) mice. In both the Min mutant and chemically induced mouse models, colon polyp formation was significantly greater in mice nullizygous for PPAR-δ. In contrast to previous reports suggesting that activation of PPAR-δ potentiates colon polyp formation, here we show that PPAR-δ attenuates colon carcinogenesis.

AB - Peroxisome proliferator-activated receptor-δ (PPAR-δ; also known as PPAR-β) is expressed at high levels in colon tumors, but its contribution to colon cancer is unclear. We examined the role of PPAR-δ in colon carcinogenesis using PPAR-δ-deficient (Ppard-/-) mice. In both the Min mutant and chemically induced mouse models, colon polyp formation was significantly greater in mice nullizygous for PPAR-δ. In contrast to previous reports suggesting that activation of PPAR-δ potentiates colon polyp formation, here we show that PPAR-δ attenuates colon carcinogenesis.

UR - https://www.scopus.com/pages/publications/2442708845

UR - https://www.scopus.com/pages/publications/2442708845#tab=citedBy

U2 - 10.1038/nm1026

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SN - 1078-8956

VL - 10

SP - 481

EP - 483

JO - Nature Medicine

JF - Nature Medicine

IS - 5

ER -

Peroxisome proliferator-activated receptor-δ attenuates colon carcinogenesis

Abstract

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