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组蛋白去乙酰化酶 6 通过微小 RNA-206 调控促进子宫内膜癌进展通过 PTEN/AKT/mTOR 通路。

HDAC6, modulated by miR-206, promotes endometrial cancer progression through the PTEN/AKT/mTOR pathway.

机构信息

Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, Shandong, China.

West China School of Medicine, Sichuan University, Chengdu, Sichuan, China.

出版信息

Sci Rep. 2020 Feb 27;10(1):3576. doi: 10.1038/s41598-020-60271-4.

DOI:10.1038/s41598-020-60271-4
PMID:32107418
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7046652/
Abstract

Endometrial cancer (EC) is the sixth most common cancer in women. Since early EC has a good prognosis, identifying methods for early diagnosis is valuable. Here, we aimed to study the role of HDAC6, which has been indicated important in many kinds of cancers, in EC diagnosis and therapy. First, the expression levels of HDAC6 in EC tissues and cells were measured by qRT-PCR and Western blotting, and through bioinformatics and dual luciferase assays, HDAC6 was found to be a direct target of miR-206. Then, CCK-8, colony formation, wound healing, and Transwell assays were performed; these results indicated that HDAC6 promoted EC cell proliferation, metastasis and invasion, while miR-206 produced the opposite effects. In addition, rescue assays verified that the effect of miR-206 could be reversed by HDAC6, and global gene expression analysis confirmed the relationship between miR-206 and HDAC6. Finally, we measured the levels of PTEN, p-AKT and p-mTOR and other key molecules and speculated that miR-206 might target HDAC6 to suppress EC progression via the PTEN/AKT/mTOR pathway. In conclusion, downregulation of miR-206 and upregulation of HDAC6 in EC may predict poor prognosis, and as the target gene of miR-206, HDAC achieves its carcinogenic effect through the PTEN/AKT/mTOR pathway.

摘要

子宫内膜癌（EC）是女性中第六种最常见的癌症。由于早期 EC 具有良好的预后，因此确定早期诊断的方法具有重要价值。在这里，我们旨在研究 HDAC6 的作用，HDAC6 在许多种癌症中都很重要。首先，通过 qRT-PCR 和 Western blot 测量了 EC 组织和细胞中 HDAC6 的表达水平，并通过生物信息学和双荧光素酶测定，发现 HDAC6 是 miR-206 的直接靶标。然后，进行了 CCK-8、集落形成、伤口愈合和 Transwell 测定；这些结果表明 HDAC6 促进了 EC 细胞的增殖、转移和侵袭，而 miR-206 则产生了相反的效果。此外，挽救实验验证了 miR-206 的作用可以被 HDAC6 逆转，并且全基因表达分析证实了 miR-206 和 HDAC6 之间的关系。最后，我们测量了 PTEN、p-AKT 和 p-mTOR 等关键分子的水平，并推测 miR-206 可能通过 PTEN/AKT/mTOR 通路靶向 HDAC6 来抑制 EC 进展。总之，EC 中 miR-206 的下调和 HDAC6 的上调可能预示着不良预后，并且作为 miR-206 的靶基因，HDAC6 通过 PTEN/AKT/mTOR 通路发挥致癌作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375b/7046652/547766d43198/41598_2020_60271_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375b/7046652/afe5f675581c/41598_2020_60271_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375b/7046652/91a9f2da3a28/41598_2020_60271_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375b/7046652/b5f03588b9e4/41598_2020_60271_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375b/7046652/b71ab98cb52a/41598_2020_60271_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375b/7046652/f14920dd19a7/41598_2020_60271_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375b/7046652/547766d43198/41598_2020_60271_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375b/7046652/afe5f675581c/41598_2020_60271_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375b/7046652/91a9f2da3a28/41598_2020_60271_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375b/7046652/b5f03588b9e4/41598_2020_60271_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375b/7046652/b71ab98cb52a/41598_2020_60271_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375b/7046652/f14920dd19a7/41598_2020_60271_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/375b/7046652/547766d43198/41598_2020_60271_Fig6_HTML.jpg

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