期刊
CANCER BIOLOGY & THERAPY
卷 22, 期 5-6, 页码 372-380出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15384047.2021.1939638
关键词
Cancer stem-like cells; FGFR; EMT; differentiation; esophageal squamous cell carcinoma
类别
资金
- Japan Society for the Promotion of Science, KAKENHI [18K07959, 20K17039]
- Grants-in-Aid for Scientific Research [20K17039, 18K07959] Funding Source: KAKEN
Fibroblast growth factors (FGFs) and their receptors (FGFRs) play an important role in maintaining cancer stem-like cells in esophageal squamous cell carcinoma (ESCC). This study reveals that FGFR2, particularly the IIIb isoform, is highly expressed in non-CSCs, inducing keratinocyte differentiation and decreasing CSC populations. Analysis using The Cancer Genome Atlas (TCGA) dataset shows a significant correlation between FGFR2 expression and cancer cell differentiation in ESCC clinical samples, suggesting FGFR2-AKT signaling as a potential therapeutic target for ESCC.
Fibroblast growth factors (FGFs) and their receptors (FGFRs) are important for signaling to maintain cancer stem-like cells (CSCs) in esophageal squamous cell carcinoma (ESCC). However, which FGF receptor, 1, 2, 3, 4, and L1, is essential or whether FGFRs have distinct different roles in ESCC-CSCs is still in question. This study shows that FGFR2, particularly the IIIb isoform, is highly expressed in non-CSCs. Non-CSCs have an epithelial phenotype, and such cells are more differentiated in ESCC. Further, FGFR2 induces keratinocyte differentiation through AKT but not MAPK signaling and diminishes CSC populations. Conversely, knockdown of FGFR2 induces epithelial-mesenchymal transition (EMT) and enriches CSC populations in ESCC. Finally, data analysis using The Cancer Genome Atlas (TCGA) dataset shows that expression of FGFR2 significantly correlated with cancer cell differentiation in clinical ESCC samples. The present study shows that each FGFR has a distinct role and FGFR2-AKT signaling is a key driver of keratinocyte differentiation in ESCC. Activation of FGFR2-AKT signaling could be a future therapeutic option targeting CSC in ESCC.
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