Coming of Age for Autotaxin and Lysophosphatidate Signaling: Clinical Applications for Preventing, Detecting and Targeting Tumor-Promoting Inflammation.
Coming of Age for Autotaxin and Lysophosphatidate Signaling: Clinical Applications for Preventing, Detecting and Targeting Tumor-Promoting Inflammation.
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DOI:
10.3390/cancers10030073
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发表时间:
2018-03-15
期刊:
影响因子:
5.2
通讯作者:
Brindley DN
中科院分区:
文献类型:
--
作者:
Benesch MGK;MacIntyre ITK;McMullen TPW;Brindley DN
A quarter-century after the discovery of autotaxin in cell culture, the autotaxin-lysophosphatidate (LPA)-lipid phosphate phosphatase axis is now a promising clinical target for treating chronic inflammatory conditions, mitigating fibrosis progression, and improving the efficacy of existing cancer chemotherapies and radiotherapy. Nearly half of the literature on this axis has been published during the last five years. In cancer biology, LPA signaling is increasingly being recognized as a central mediator of the progression of chronic inflammation in the establishment of a tumor microenvironment which promotes cancer growth, immune evasion, metastasis, and treatment resistance. In this review, we will summarize recent advances made in understanding LPA signaling with respect to chronic inflammation and cancer. We will also provide perspectives on the applications of inhibitors of LPA signaling in preventing cancer initiation, as adjuncts extending the efficacy of current cancer treatments by blocking inflammation caused by either the cancer or the cancer therapy itself, and by disruption of the tumor microenvironment. Overall, LPA, a simple molecule that mediates a plethora of biological effects, can be targeted at its levels of production by autotaxin, LPA receptors or through LPA degradation by lipid phosphate phosphatases. Drugs for these applications will soon be entering clinical practice.
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DOI:
10.1016/j.bbalip.2012.08.015
发表时间:
2013-01
期刊:
Biochimica et biophysica acta
影响因子:
--
作者:
Brindley DN;Lin FT;Tigyi GJ
通讯作者:
Tigyi GJ
影响因子:
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作者:
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通讯作者:
Brindley DN
影响因子:
4.8
作者:
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通讯作者:
Brindley, David N.
影响因子:
37.8
作者:
Bouchareb, Rihab;Mahmut, Ablajan;Mathieu, Patrick
通讯作者:
Mathieu, Patrick
影响因子:
--
作者:
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通讯作者:
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