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人类 TRAIL 基因的调控。

Regulation of the human TRAIL gene.

机构信息

Laboratory of Translational Oncology and Experimental Cancer Therapeutics, Department of Medicine (Hematology/Oncology), Penn State Hershey Cancer Institute, Hershey, PA, USA.

出版信息

Cancer Biol Ther. 2012 Oct;13(12):1143-51. doi: 10.4161/cbt.21354. Epub 2012 Aug 15.

DOI:10.4161/cbt.21354
PMID:22892844
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3469471/
Abstract

TRAIL is a member of the TNF superfamily that induces tumor-selective cell death by engaging the pro-apoptotic death receptors DR4 and DR5. The antitumor potential of the TRAIL pathway has been targeted by several therapeutic approaches including recombinant TRAIL and TRAIL-receptor agonist antibodies among others. Interest in sensitizing tumor cells to TRAIL-mediated apoptosis has driven investigations of TRAIL-receptor gene regulation, though regulation of the TRAIL gene has been less studied. Physiologically, TRAIL serves as a pro-apoptotic effector molecule in the immune surveillance of cancer that is conditionally expressed by immune cells upon stimulation via an interferon-response element that was identified in early studies of the TRAIL gene promoter. Here, we map the TRAIL gene promoter and review studies of TRAIL gene regulation that involve several modalities of gene regulation including transcription factors, epigenetics, single-nucleotide polymorphisms and functionally distinct isoforms.

摘要

TRAIL 是 TNF 超家族的一员，通过与促凋亡死亡受体 DR4 和 DR5 结合，诱导肿瘤选择性细胞死亡。几种治疗方法包括重组 TRAIL 和 TRAIL 受体激动剂抗体等，都将 TRAIL 通路的抗肿瘤潜力作为靶向。为了提高肿瘤细胞对 TRAIL 介导的细胞凋亡的敏感性，人们对 TRAIL 受体基因调控进行了研究，尽管对 TRAIL 基因的调控研究较少。从生理上讲，TRAIL 是癌症免疫监视中的一种促凋亡效应分子，在早期对 TRAIL 基因启动子的研究中发现，免疫细胞在受到干扰素反应元件刺激时会条件性表达。在这里，我们绘制了 TRAIL 基因启动子图谱，并回顾了涉及多种基因调控方式的 TRAIL 基因调控研究，包括转录因子、表观遗传学、单核苷酸多态性和功能不同的同工型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f736/3469471/13430b264fa1/cbt-13-1143-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f736/3469471/f795dc3c08f2/cbt-13-1143-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f736/3469471/0ce2aa7c6c97/cbt-13-1143-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f736/3469471/4a99199b7abc/cbt-13-1143-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f736/3469471/3f916b25c650/cbt-13-1143-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f736/3469471/13430b264fa1/cbt-13-1143-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f736/3469471/f795dc3c08f2/cbt-13-1143-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f736/3469471/0ce2aa7c6c97/cbt-13-1143-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f736/3469471/4a99199b7abc/cbt-13-1143-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f736/3469471/3f916b25c650/cbt-13-1143-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f736/3469471/13430b264fa1/cbt-13-1143-g5.jpg

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