Abstract
Esophageal cancer is the eighth most common malignant tumor worldwide, of which esophageal squamous cell carcinoma (ESCC) is the dominant histological subtype. A drug shortage for ESCC therapy triggered us to explore the roles of fibroblast growth factor receptor 2 (FGFR2) and its upstream regulator miR-671-5p in ESCC progression. We compared the levels of FGFR2 and miR-671-5p between human ESCC tissues and their matched normal esophageal tissues and found an association between higher levels of FGFR2 and lower levels of miR-671-5p in ESCC tissues. High levels of FGFR2 resulted in the activation of the ERK and AKT pathways and a promotion of ESCC progression. High levels of miR-671-5p specifically reduced the expression of FGFR2 and suppressed ESCC progression in both in vitro and in vivo models. Therefore, suppressing FGFR2 and enhancing miR-671-5p expression may be the right approaches for ESCC therapy.
Keywords:
ESCC; FGFR2; miR-671-5p; tumor progression.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
3' Untranslated Regions / genetics
-
Animals
-
Cell Line, Tumor
-
Cell Movement / genetics
-
Cell Movement / physiology
-
Cell Proliferation / genetics
-
Cell Proliferation / physiology
-
Disease Progression
-
Esophageal Neoplasms / genetics
-
Esophageal Neoplasms / metabolism*
-
Esophageal Neoplasms / pathology
-
Esophageal Squamous Cell Carcinoma / genetics
-
Esophageal Squamous Cell Carcinoma / metabolism*
-
Esophageal Squamous Cell Carcinoma / pathology
-
Gene Expression Regulation, Neoplastic / genetics
-
Gene Expression Regulation, Neoplastic / physiology
-
Humans
-
Immunoblotting
-
In Vitro Techniques
-
Mice
-
Mice, Inbred BALB C
-
MicroRNAs / genetics
-
MicroRNAs / metabolism*
-
Receptor, Fibroblast Growth Factor, Type 2 / genetics
-
Receptor, Fibroblast Growth Factor, Type 2 / metabolism*
-
Signal Transduction / genetics
-
Signal Transduction / physiology
Substances
-
3' Untranslated Regions
-
MIRN671 microRNA, human
-
MicroRNAs
-
FGFR2 protein, human
-
Receptor, Fibroblast Growth Factor, Type 2