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Int J Biol Sci 2019; 15(9):1892-1904. doi:10.7150/ijbs.32429 This issue

Research Paper

miR-671-5p Blocks The Progression Of Human Esophageal Squamous Cell Carcinoma By Suppressing FGFR2

Xiaoyan Li1,2,3*, Changjun Nie1,2,3*, Baoqing Tian1,2,3, Xuan Tan1,2,3, Wei Han1,2,3, Jiakang Wang4, Yuan Jin1,2,3, Yadan Li1,2,3, Xinyuan Guan5, An Hong1,2,3✉, Xiaojia Chen1,2,3✉

1. Institute of Biomedicine & Department of cell Biology, Jinan University, Guangzhou, Guangdong, 510632, P. R. China.
2. National Engineering Research Center of Genetic Medicine, Guangzhou, Guangdong, 510632, P. R. China.
3. Guangdong Provincial Key Laboratory of Bioengineering Medicine, Guangzhou, Guangdong, 510632, P. R. China.
4. Cancer Center of Guangzhou Medical University, Guangzhou, Guangdong, 510090, P. R. China.
5. Department of Clinical Oncology, University of Hong Kong, Hong Kong, China
*Both authors contributed to the work equally.

✉ Corresponding author: Xiaojia Chen and An Hong, Institute of Biomedicine & Department of cell Biology, Jinan University, National Engineering Research Center of Genetic Medicine, and Guangdong Provincial Key Laboratory of Bioengineering Medicine More

This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.
Citation:
Li X, Nie C, Tian B, Tan X, Han W, Wang J, Jin Y, Li Y, Guan X, Hong A, Chen X. miR-671-5p Blocks The Progression Of Human Esophageal Squamous Cell Carcinoma By Suppressing FGFR2. Int J Biol Sci 2019; 15(9):1892-1904. doi:10.7150/ijbs.32429. Available from https://www.ijbs.com/v15p1892.htm

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Abstract

Graphic 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: FGFR2, miR-671-5p, ESCC, tumor progression

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