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表观遗传学在非小细胞肺癌中 CXCL（ELR+）趋化因子调控中的作用。

Epigenetics underpinning the regulation of the CXC (ELR+) chemokines in non-small cell lung cancer.

机构信息

Thoracic Oncology Research Group, Institute of Molecular Medicine, Trinity College, Dublin, Ireland.

出版信息

PLoS One. 2011 Jan 27;6(1):e14593. doi: 10.1371/journal.pone.0014593.

DOI:10.1371/journal.pone.0014593
PMID:21298036
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3029265/
Abstract

BACKGROUND

Angiogenesis may play a role in the pathogenesis of Non-Small Cell Lung cancer (NSCLC). The CXC (ELR(+)) chemokine family are powerful promoters of the angiogenic response.

METHODS

The expression of the CXC (ELR(+)) family members (CXCL1-3/GROα-γ, CXCL8/IL-8, CXCR1/2) was examined in a series of resected fresh frozen NSCLC tumours. Additionally, the expression and epigenetic regulation of these chemokines was examined in normal bronchial epithelial and NSCLC cell lines.

RESULTS

Overall, expression of the chemokine ligands (CXCL1, 2, 8) and their receptors (CXCR1/2) were down regulated in tumour samples compared with normal, with the exception of CXCL3. CXCL8 and CXCR1/2 were found to be epigenetically regulated by histone post-translational modifications. Recombinant CXCL8 did not stimulate cell growth in either a normal bronchial epithelial or a squamous carcinoma cell line (SKMES-1). However, an increase was observed at 72 hours post treatment in an adenocarcinoma cell line.

CONCLUSIONS

CXC (ELR(+)) chemokines are dysregulated in NSCLC. The balance of these chemokines may be critical in the tumour microenvironment and requires further elucidation. It remains to be seen if epigenetic targeting of these pathways is a viable therapeutic option in lung cancer treatment.

摘要

背景

血管生成可能在非小细胞肺癌（NSCLC）的发病机制中起作用。CXC（ELR（+））趋化因子家族是血管生成反应的强大促进剂。

方法

在一系列切除的新鲜冷冻 NSCLC 肿瘤中检查了 CXC（ELR（+））家族成员（CXCL1-3/GROα-γ、CXCL8/IL-8、CXCR1/2）的表达。此外，还在正常支气管上皮细胞和 NSCLC 细胞系中检查了这些趋化因子的表达和表观遗传调控。

结果

总体而言，与正常相比，肿瘤样本中趋化因子配体（CXCL1、2、8）及其受体（CXCR1/2）的表达下调，除 CXCL3 外。CXCL8 和 CXCR1/2 被发现通过组蛋白翻译后修饰进行表观遗传调控。重组 CXCL8 并未刺激正常支气管上皮或鳞状癌细胞系（SKMES-1）中的细胞生长。然而，在腺癌细胞系中，在治疗后 72 小时观察到增加。

结论

CXC（ELR（+））趋化因子在 NSCLC 中失调。这些趋化因子的平衡可能在肿瘤微环境中至关重要，需要进一步阐明。尚不清楚针对这些途径的表观遗传靶向是否是肺癌治疗的可行治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50dc/3029265/aaeb14b0fad9/pone.0014593.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50dc/3029265/c45ae07f6f6b/pone.0014593.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50dc/3029265/ac1426b595ab/pone.0014593.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50dc/3029265/fc57446e3fc2/pone.0014593.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50dc/3029265/dcafce96e967/pone.0014593.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50dc/3029265/1660705c01ec/pone.0014593.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50dc/3029265/aaeb14b0fad9/pone.0014593.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50dc/3029265/c45ae07f6f6b/pone.0014593.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50dc/3029265/ac1426b595ab/pone.0014593.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50dc/3029265/fc57446e3fc2/pone.0014593.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50dc/3029265/dcafce96e967/pone.0014593.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50dc/3029265/1660705c01ec/pone.0014593.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50dc/3029265/aaeb14b0fad9/pone.0014593.g006.jpg

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