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胸腺瘤伴或不伴重症肌无力的基因表达谱改变与重症肌无力发病的核因子-κB/自身免疫调节因子通路有关。

Alteration in gene expression profile of thymomas with or without myasthenia gravis linked with the nuclear factor-kappaB/autoimmune regulator pathway to myasthenia gravis pathogenesis.

机构信息

Department of Endoscopy, Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, China.

Department of Neurology, Tianjin Medical University General Hospital, Tianjin, China.

出版信息

Thorac Cancer. 2019 Mar;10(3):564-570. doi: 10.1111/1759-7714.12980. Epub 2019 Feb 7.

DOI:10.1111/1759-7714.12980
PMID:30734484
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6397909/
Abstract

BACKGROUND

To investigate the gene expression profile of a set of candidate genes for a better understanding of the molecular mechanism underlying the pathogenesis of thymoma with or without myasthenia gravis.

METHODS

Thymoma patients and thymoma patients with myasthenia gravis were analyzed using microarray profiling to identify significant changes in gene expression of autoimmune regulator pathway genes including AIRE, IL-7R, CHRNA3, SYMD1, THRA, and CAV3.

RESULTS

Across all of our samples, we found that 1484 mRNAs were upregulated and 770 were downregulated in thymoma patients compared with thymoma with myasthenia gravis patients. Gene ontology and pathway analysis revealed that a large number of genes participated in cellular functions for humoral immune response, sequence-specific DNA binding RNA polymerase II transcription factor activity, positive regulation of gene expression, regulation of neuron projection development, extracellular ligand-gated ion channel activity, positive regulation of striated muscle cell differentiation, and regulation of nuclear factor-kappaB import into the nucleus.

CONCLUSION

Our results revealed genetic differences between thymomas and myasthenia gravis, and identified the key candidate genes/pathways for molecular mechanism.

摘要

背景

为了更好地了解重症肌无力伴胸腺瘤和不伴重症肌无力胸腺瘤发病机制的分子机制，我们对一组候选基因的基因表达谱进行了研究。

方法

采用微阵列分析方法对胸腺瘤患者和重症肌无力伴胸腺瘤患者进行分析，以鉴定自身免疫调节途径基因（如 AIRE、IL-7R、CHRNA3、SYMD1、THRA 和 CAV3）的基因表达的显著变化。

结果

在我们所有的样本中，我们发现与重症肌无力伴胸腺瘤患者相比，胸腺瘤患者中有 1484 个 mRNA 上调，770 个 mRNA 下调。基因本体论和通路分析显示，大量基因参与了体液免疫反应、序列特异性 DNA 结合 RNA 聚合酶Ⅱ转录因子活性、基因表达的正调控、神经元投射发育的调控、细胞外配体门控离子通道活性、有条纹肌肉细胞分化的正调控以及核因子κB 向核内导入的调控等细胞功能。

结论

我们的研究结果揭示了胸腺瘤和重症肌无力之间的遗传差异，并确定了用于分子机制的关键候选基因/通路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8eb/6397909/1b4f4055b87a/TCA-10-564-g015.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8eb/6397909/30e662d64fd4/TCA-10-564-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8eb/6397909/d316f46ea639/TCA-10-564-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8eb/6397909/958c43910898/TCA-10-564-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8eb/6397909/1b4f4055b87a/TCA-10-564-g015.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8eb/6397909/30e662d64fd4/TCA-10-564-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8eb/6397909/d316f46ea639/TCA-10-564-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8eb/6397909/958c43910898/TCA-10-564-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8eb/6397909/1b4f4055b87a/TCA-10-564-g015.jpg

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