Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 234, Issue 12, Pages 23596-23607Publisher
WILEY
DOI: 10.1002/jcp.28928
Keywords
BARX2; epithelial-mesenchymal transition; metastasis; miR-942; NSCLC
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Funding
- Jiangsu Social Development Project [BE2018726]
- Natural Science Foundation of Jiangsu Province [BK20171484]
- National Natural Science Foundation of China [81874230]
- Summit of the Six Top Talents Program of Jiangsu Province [2017-WSN-179, KYCX18_1483]
- Postgraduate Research & Practice Innovation Program of Jiangsu Province
- Priority Academic Program Development of Jiangsu Higher Education Institutions [JX10231801]
- Project of Invigorating Health Care through Science, Technology, and Education [QNRC2016856]
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Epithelial-mesenchymal transition (EMT) has an important function in cancer. Recently, microRNAs have been reported to be involved in EMT by regulating target genes. miR-942 is considered a novel oncogene in esophageal squamous cell carcinoma. However, its role innon-small-cell lung cancer (NSCLC) has not been investigated. In this study, the expression of miR-942 in NSCLC patients tumor and paired adjacent tissues were assessed by quantitative real-time polymerase chain reactionand in situ hybridization. Transwell, wound healing, tube formation, and tail vein xenograft assays were conducted to assess miR-942 ' s function in NSCLC. Potential miR-942 targets were confirmed using dual-luciferase reporter assays, immunohistochemistry, immunoblot, and rescue experiments. The results showed miR-942 is relatively highly expressed in human NSCLC tissues and cells. In vitro assays demonstrated that overexpression of miR-942 promoted cell migration, invasion, and angiogenesis. Tail vein xenograft assays suggested that miR-942 contributed to NSCLC metastasis in vivo. Three bioinformatics software was searched, and BARX2 was predicted as a downstream target of miR-942. Direct interaction between them was validated by dual-luciferase assays. Rescue experiments further confirmed that BARX2 overexpression could reverse functional changes caused by miR-942. Moreover, miR-942 increased EMT-associated proteins N-cadherin and vimentin by inhibiting BARX2, while E-cadherin expression is reduced. In summary, this study reveals that miR-942 induces EMT-related metastasis by directly targeting BARX2, which may provide a potential therapeutic strategy for NSCLC.
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