Open AccessMicro RNA 26b promotes colorectal cancer metastasis by downregulating phosphatase and tensin homolog and wingless‐type MMTV integration site family member 5A
Author(s) -
Fan Dejun,
Lin Xutao,
Zhang Feng,
Zhong Weijie,
Hu Jiancong,
Chen Yufeng,
Cai Zerong,
Zou Yifeng,
He Xiaowen,
Chen Xiuting,
Lan Ping,
Wu Xiaojian
Publication year - 2018
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.13451
Subject(s) - tensin , pten , cancer research , metastasis , wnt signaling pathway , biology , microrna , colorectal cancer , ectopic expression , cancer , downregulation and upregulation , cell culture , pi3k/akt/mtor pathway , signal transduction , microbiology and biotechnology , gene , genetics
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 micro RNA 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 ( WNT 5A). 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 WNT 5A, and may represent a therapeutic target for metastatic CRC .