Journal
ONCOLOGY REPORTS
Volume 40, Issue 2, Pages 704-714Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/or.2018.6482
Keywords
fibroblast growth factor 18; MDA-MB-231; proliferation; migration; invasion; ERK; EMT
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Funding
- Talents Planning of Six Summit Fields of Jiangsu Province [WSW-026]
- Maternal and Child Health Research Projects of Jiangsu Province [F201678]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD) [JX10231801]
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Fibroblast growth factor 18 (FGF18) increases cell motility and invasion in colon tumors, and is linked with ovarian and lung tumors. Furthermore, the increased expression of FGF18 mRNA and protein has been associated with poor overall survival in cancer patients. However, its function has not been investigated in breast cancer. In the present study, we demonstrated that FGF18 promoted cell growth and metastasis in vitro and stimulated tumor growth in xenograft models in vivo. FGF18 mediated the proliferation of MDA-MB-231 cells via the ERK/c-Myc signaling pathway and induced epithelial-to-mesenchymal transition (EMT) factors to promote cancer migration and invasion. The decreased expression of FGF18 was strongly correlated with the loss/reduction of p-ERK, c-Myc, N-cadherin, vimentin and Snail 1 protein in MDA-MB-231 cells. Collectively, our results indicated that FGF18 played an important role in the growth and metastasis of breast cancer via the ERK/c-Myc signaling pathway and EMT, indicating that FGF18 may be a potential molecular treatment target for breast cancer.
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