期刊
ONCOGENESIS
卷 8, 期 -, 页码 -出版社
SPRINGERNATURE
DOI: 10.1038/s41389-019-0151-1
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资金
- National Key R&D Program of China [2016YFC1303300]
- Shanghai Chest Hospital Project of Collaborative Innovation [YJXT20190105, YJXT20190209]
- Clinical Research Plan of SHDC [16CR3005A]
- Shanghai Science and Technology Commission guidance projects [18411968200]
- Medical-Engineering Joint Funds of Shanghai Jiao Tong University [YG2017MS81]
- Shanghai Youth Top Talent Project
- National Natural Science Foundation of China [81672272, 81773115]
- National Key Grant of China [2016YFC0906400]
- Key project of Shanghai Health and Family Planning [201540365]
- Shanghai Municipal Science and Technology Commission Research Project [17431906103]
- Shanghai Scientific Research Projects [14140902800]
- AstraZeneca Pharmaceutical Company
MicroRNA (miRNA) and fibroblast growth factor receptor 1 (FGFR1) dysregulation are considered to play an important role in tumor proliferation, invasion, and metastasis. However, the regulatory mechanism between miRNAs and FGFR1 in lung cancer remains unclear and extremely critical. miR-214-3p was sharply decreased and showed a significantly negative correlation with FGFR1 in lung cancer patients (n = 30). Luciferase reporter assay confirmed that miR-214-3p could downregulate FGFR1 by directly targeting 3'-untranslated region (UTR). miR-214-3p inhibited the processes of epithelial-mesenchymal transition and Wnt/MAPK/AKT (Wnt/mitogen-activated protein kinase/AKT) signaling pathway by targeting FGFR1. Moreover, miR-214-3p not only established a negative feedback regulation loop with FGFR1 through ERK (extracellular signal-regulated kinase) but also developed a synergism with FGFR1 inhibitor AZD4547. In conclusion, our study demonstrated the regulatory mechanism between miR-214-3p and FGFR1 in lung cancer. miR-214-3p acts as a vital target in FGFR1-amplified lung cancer by forming a miR-214-3p-FGFR1-Wnt/MAPK/AKT signaling pathway network. Co-targeting miR-214-3p and FGFR1 could provide greater benefits to patients with FGFR1-amplified lung cancer.
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