MicroRNA 26b promotes colorectal cancer metastasis by downregulating phosphatase and tensin homolog and wingless‐type MMTV integration site family member 5A. Issue 2 (20th December 2017)

• Record Type: Journal Article
• Authors: Fan, Dejun; Lin, Xutao; Zhang, Feng; Zhong, Weijie; Hu, Jiancong; Chen, Yufeng; Cai, Zerong; Zou, Yifeng; He, Xiaowen; Chen, Xiuting; Lan, Ping; Wu, Xiaojian
• Is Part Of: Cancer science. Volume 109:Issue 2(2018)
• Page Start: 354
• Page End: 362
• Publication Date: 2017-12-20
• Subjects: colorectal cancer -- invasion and metastasis -- miR‐26b -- PTEN -- WNT5A; Cancer -- Periodicals; Neoplasms -- Periodicals; Research -- Periodicals; Electronic journals; 616.994005
• DOI: 10.1111/cas.13451
• Languages: English
• ISSNs: 1347-9032

Abstract

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. Abstract : Ectopic overexpression of miR‐26b promoted EMT and stem cell‐like phenotype in vitro in CRC cell lines. Furthermore, miR‐26b directly suppressed PTEN and WNT5A. This demonstrates that miR‐26b promotes colorectal cancer metastasis by downregulating PTEN and WNT5A and may represent a therapeutic target for early metastatic colorectal cancer.