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首页> 外文期刊>Cancer Cell >Prostaglandin E(2) promotes colorectal adenoma growth via transactivation of the nuclear peroxisome proliferator-activated receptor delta.
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Prostaglandin E(2) promotes colorectal adenoma growth via transactivation of the nuclear peroxisome proliferator-activated receptor delta.

机译：前列腺素E（2）通过反式激活核过氧化物酶体增殖物激活受体δ促进结直肠腺瘤生长。

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摘要

Cyclooxygenase-derived prostaglandin E(2) (PGE(2)) is the predominant prostanoid found in most colorectal cancers (CRC) and is known to promote colon carcinoma growth and invasion. However, the key downstream signaling pathways necessary for PGE(2)-induced intestinal carcinogenesis are unclear. Here we report that PGE(2) indirectly transactivates PPARdelta through PI3K/Akt signaling, which promotes cell survival and intestinal adenoma formation. We also found that PGE(2) treatment of Apc(min) mice dramatically increased intestinal adenoma burden, which was negated in Apc(min) mice lacking PPARdelta. We demonstrate that PPARdelta is a focal point of crosstalk between the prostaglandin and Wnt signaling pathways which results in a shift from cell death to cell survival, leading to increased tumor growth.
机译：环氧合酶衍生的前列腺素E（2）（PGE（2））是大多数大肠癌（CRC）中发现的主要类前列腺素，已知可促进结肠癌的生长和侵袭。但是，尚不清楚PGE（2）诱导肠癌发生所必需的关键下游信号通路。在这里我们报告PGE（2）通过PI3K / Akt信号间接激活PPARdelta，从而促进细胞存活和肠腺瘤的形成。我们还发现，PGE（2）对Apc（min）小鼠的治疗显着增加了肠道腺瘤的负担，而在缺乏PPARdelta的Apc（min）小鼠中则被否定了。我们证明PPARdelta是前列腺素和Wnt信号通路之间的串扰焦点，其导致从细胞死亡转移到细胞存活，从而导致肿瘤生长增加。

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