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miR-200b/200a/429簇通过靶向ING5促进卵巢癌发展。

miR-200b/200a/429 Cluster Stimulates Ovarian Cancer Development by Targeting ING5.

作者信息

Guan Wei, Cui Huiling, Huang Ping, Chun Wan Joo, Lee Jin-Won, Kim Heasung, Zou Hua

机构信息

Cancer Center, Daping Hospital, Third Military Medical University, Chongqing 400042, China.

College of Pharmacy, Yanbian University, Yanji 133002, Jilin Province, China.

出版信息

J Oncol. 2020 Apr 22;2020:3404059. doi: 10.1155/2020/3404059. eCollection 2020.

DOI:10.1155/2020/3404059
PMID:32377191
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7193301/
Abstract

Ovarian cancer is the second most common gynaecological malignancy, and microRNAs (miRNAs) play important role in the cancer development. Here, we found that the level of miR-200b/200a/429 was significantly increased in serum and tumor tissues of patients with stage-I ovarian cancer. Consistent with these results, we detected increased expression levels of miR-200b/200a/429 in ovarian cancer cell lines compared with the human nontumorigenic ovarian epithelial cell line T80. The overexpression of miR-200b/200a/429 in T80 cells stimulated proliferation and caused their growth in soft agar and tumor formation in nude mice. Furthermore, we determined that miR-200b/200a/429 targets inhibitor of growth family 5 (ING5) and that the overexpression of ING5 can block miR-200b/200a/429-induced T80 cell transformation and tumorigenesis. Our findings suggest that miR-200b/200a/429 may be a useful biomarker for the early detection of ovarian cancer and that miR-200b/200a/429 significantly contributes to ovarian cancer development through ING5.

摘要

卵巢癌是第二常见的妇科恶性肿瘤，而微小RNA（miRNA）在癌症发展中发挥着重要作用。在此，我们发现I期卵巢癌患者血清和肿瘤组织中miR-200b/200a/429水平显著升高。与这些结果一致，我们检测到与人类非致瘤性卵巢上皮细胞系T80相比，卵巢癌细胞系中miR-200b/200a/429的表达水平升高。在T80细胞中过表达miR-200b/200a/429可刺激增殖，并使其在软琼脂中生长以及在裸鼠体内形成肿瘤。此外，我们确定miR-200b/200a/429靶向生长抑制家族5（ING5），并且ING5的过表达可阻断miR-200b/200a/429诱导的T80细胞转化和肿瘤发生。我们的研究结果表明，miR-200b/200a/429可能是卵巢癌早期检测的有用生物标志物，并且miR-200b/200a/429通过ING5对卵巢癌发展有显著贡献。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0520/7193301/6f3ab5bc3529/JO2020-3404059.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0520/7193301/52d59bcd5d84/JO2020-3404059.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0520/7193301/1d379e704a3d/JO2020-3404059.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0520/7193301/711eab75ac68/JO2020-3404059.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0520/7193301/6f3ab5bc3529/JO2020-3404059.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0520/7193301/52d59bcd5d84/JO2020-3404059.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0520/7193301/1d379e704a3d/JO2020-3404059.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0520/7193301/711eab75ac68/JO2020-3404059.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0520/7193301/6f3ab5bc3529/JO2020-3404059.004.jpg

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