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微小RNA 26b通过下调磷酸酶及张力蛋白同源物和无翅型MMTV整合位点家族成员5A促进结直肠癌转移。

MicroRNA 26b promotes colorectal cancer metastasis by downregulating phosphatase and tensin homolog and wingless-type MMTV integration site family member 5A.

作者信息

Fan Dejun, Lin Xutao, Zhang Feng, Zhong Weijie, Hu Jiancong, Chen Yufeng, Cai Zerong, Zou Yifeng, He Xiaowen, Chen Xiuting, Lan Ping, Wu Xiaojian

机构信息

Department of Colorectal Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.

Department of Gastrointestinal Endoscopy, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.

出版信息

Cancer Sci. 2018 Feb;109(2):354-362. doi: 10.1111/cas.13451. Epub 2017 Dec 20.

DOI:10.1111/cas.13451
PMID:29160937
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5797816/
Abstract

Invasion and metastasis are crucially important factors in the survival of malignant tumors. Epithelial-mesenchymal transition (EMT) is an early step in metastatic progression and the presence of cancer stem cells is closely related to tumor survival, proliferation, metastasis, and recurrence. Herein we report that ectopic overexpression of microRNA 26b (miR-26b) in colorectal cancer (CRC) cell lines promoted EMT and stem cell-like phenotypes in vitro. Furthermore, miR-26b directly targeted and suppressed multiple tumor suppressors, including phosphatase and tensin homolog (PTEN) and wingless-type MMTV integration site family member 5A (WNT5A). Notably, miR-26b is markedly upregulated in tumor samples from patients with lymphatic metastases. These results indicate that miR-26b promotes CRC metastasis by downregulating PTEN and WNT5A, and may represent a therapeutic target for metastatic CRC.

摘要

侵袭和转移是恶性肿瘤生存的关键重要因素。上皮-间质转化（EMT）是转移进程中的早期步骤，癌症干细胞的存在与肿瘤的生存、增殖、转移和复发密切相关。在此我们报告，在结直肠癌（CRC）细胞系中异位过表达微小RNA 26b（miR-26b）在体外促进了EMT和干细胞样表型。此外，miR-26b直接靶向并抑制多种肿瘤抑制因子，包括磷酸酶和张力蛋白同源物（PTEN）以及无翅型MMTV整合位点家族成员5A（WNT5A）。值得注意的是，miR-26b在有淋巴转移患者的肿瘤样本中显著上调。这些结果表明，miR-26b通过下调PTEN和WNT5A促进CRC转移，并且可能代表转移性CRC的一个治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c67/5797816/88b38d2c7265/CAS-109-354-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c67/5797816/329a714a830c/CAS-109-354-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c67/5797816/6feae18ced6c/CAS-109-354-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c67/5797816/4200a44b42cd/CAS-109-354-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c67/5797816/b248ad9a884b/CAS-109-354-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c67/5797816/5cb50ea34542/CAS-109-354-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c67/5797816/88b38d2c7265/CAS-109-354-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c67/5797816/329a714a830c/CAS-109-354-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c67/5797816/6feae18ced6c/CAS-109-354-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c67/5797816/4200a44b42cd/CAS-109-354-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c67/5797816/b248ad9a884b/CAS-109-354-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c67/5797816/5cb50ea34542/CAS-109-354-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c67/5797816/88b38d2c7265/CAS-109-354-g006.jpg

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