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全面分析新型上皮-间质转化介体及其在结直肠癌中的临床意义。

Comprehensive profiling of novel epithelial-mesenchymal transition mediators and their clinical significance in colorectal cancer.

机构信息

Department of Gastroenterological Surgery, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.

Department of Frontier Science for Cancer and Chemotherapy, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.

出版信息

Sci Rep. 2021 Jun 3;11(1):11759. doi: 10.1038/s41598-021-91102-9.

DOI:10.1038/s41598-021-91102-9
PMID:34083586
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8175715/
Abstract

Epithelial-mesenchymal transition (EMT) is a drastic phenotypic change during cancer metastasis and is one of the most important hallmarks of aggressive cancer. Although the overexpression of some specific transcription factors explains the functional alteration of EMT-induced cells, a complete picture of this biological process is yet to be elucidated. To comprehensively profile EMT-related genes in colorectal cancer, we quantified the EMT induction ability of each gene according to its similarity to the cancer stromal gene signature and termed it "mesenchymal score." This bioinformatic approach successfully identified 90 candidate EMT mediators, which are strongly predictive of survival in clinical samples. Among these candidates, we discovered that the neuronal gene ARC, possibly originating from the retrotransposon, unexpectedly plays a crucial role in EMT induction. Profiling of novel EMT mediators we demonstrated here may help understand the complexity of the EMT program and open up new avenues for therapeutic intervention in colorectal cancer.

摘要

上皮-间充质转化（EMT）是癌症转移过程中的一种剧烈表型变化，是侵袭性癌症的最重要标志之一。虽然某些特定转录因子的过表达解释了 EMT 诱导细胞的功能改变，但这一生物学过程的全貌仍有待阐明。为了全面分析结直肠癌中的 EMT 相关基因，我们根据每个基因与癌症基质基因特征的相似性来量化其 EMT 诱导能力，并将其称为“间充质评分”。这种生物信息学方法成功鉴定了 90 个候选 EMT 介质，这些介质在临床样本中对生存具有很强的预测性。在这些候选物中，我们发现神经元基因 ARC，可能来源于逆转录转座子，出人意料地在 EMT 诱导中发挥关键作用。我们在此展示的对新型 EMT 介质的分析可能有助于理解 EMT 程序的复杂性，并为结直肠癌的治疗干预开辟新途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e76/8175715/ab900d1d6fa7/41598_2021_91102_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e76/8175715/82e30e54563a/41598_2021_91102_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e76/8175715/b75d955d6469/41598_2021_91102_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e76/8175715/a57665c6d00b/41598_2021_91102_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e76/8175715/e261be36ba80/41598_2021_91102_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e76/8175715/1dc2197f63e7/41598_2021_91102_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e76/8175715/ab900d1d6fa7/41598_2021_91102_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e76/8175715/82e30e54563a/41598_2021_91102_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e76/8175715/b75d955d6469/41598_2021_91102_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e76/8175715/a57665c6d00b/41598_2021_91102_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e76/8175715/e261be36ba80/41598_2021_91102_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e76/8175715/1dc2197f63e7/41598_2021_91102_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e76/8175715/ab900d1d6fa7/41598_2021_91102_Fig6_HTML.jpg

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MicroRNA-495 confers inhibitory effects on cancer stem cells in oral squamous cell carcinoma through the HOXC6-mediated TGF-β signaling pathway.
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Pharmacological inhibition of HDAC6 improves muscle phenotypes in dystrophin-deficient mice by downregulating TGF-β via Smad3 acetylation.组蛋白去乙酰化酶 6 的药理学抑制通过乙酰化 Smad3 下调 TGF-β改善肌营养不良症小鼠的肌肉表型。
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