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辐射抗性、侵袭性和转移性是炎症事件,可以被脂氧素 A4 抑制。

Radiation resistance, invasiveness and metastasis are inflammatory events that could be suppressed by lipoxin A4.

机构信息

UND Life Sciences, Shaker Heights, OH 44120, USA.

出版信息

Prostaglandins Leukot Essent Fatty Acids. 2012 Jan-Feb;86(1-2):3-11. doi: 10.1016/j.plefa.2011.09.008. Epub 2011 Oct 19.

DOI:10.1016/j.plefa.2011.09.008
PMID:22014542
Abstract

Radiation induces overexpression and activity of the MET oncogene that, in turn, enhances the production of prostaglandin E(2), a pro-inflammatory molecule. Prostaglandin E(2) promotes tumor cell invasion, prevents apoptosis, enhances their metastasis and causes radioresistance. It is proposed that lipoxin A(4), a potent endogenous anti-inflammatory molecule, opposes the actions of prostaglandin E(2) and thus, could promote radiosensitivity, suppress tumor cell proliferation, invasiveness and suppress metastasis. Thus, methods designed to enhance endogenous lipoxin A(4) formation or its synthetic analogs may be useful in the management of cancer.

摘要

辐射会诱导 MET 癌基因的过度表达和激活,进而增强促炎分子前列腺素 E2(PGE2)的产生。前列腺素 E2 促进肿瘤细胞侵袭,阻止细胞凋亡,增强其转移能力并导致放射抵抗。有人提出,脂氧素 A4(一种有效的内源性抗炎分子)对抗前列腺素 E2 的作用,因此可能促进放射敏感性,抑制肿瘤细胞增殖、侵袭和转移。因此,旨在增强内源性脂氧素 A4 形成或其合成类似物的方法可能有助于癌症的治疗。

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