Research Papers:
SATB1 plays an oncogenic role in esophageal cancer by up-regulation of FN1 and PDGFRB
PDF | HTML | Supplementary Files | How to cite
Metrics: PDF 2829 views | HTML 3112 views | ?
Abstract
Guiqin Song1,2,5,*, Kang Liu2,3,*, Xiaolin Yang1,2, Bo Mu1, Junbao Yang1, Lang He2,3, Xin Hu3, Qiujiang Li4, Yunxia Zhao4, Xiaoming Cai1, Gang Feng2,3
1Department of Biology, North Sichuan Medical College, Nanchong, Sichuan, P.R. China
2Institute of Tissue Engineering and Stem Cells, The Second Clinical Medical College of North Sichuan Medical College, Nanchong Central Hospital, Nanchong, Sichuan, P.R. China
3Biotherapy Center, Nanchong Central Hospital, Nanchong, Sichuan, P.R. China
4Clinical college of North Sichuan Medical College, Nanchong, Sichuan, P.R. China
5State Key Laboratory of Biotherapy, Sichuan University, Chengdu, Sichuan, P.R. China
*These authors contributed equally to this work
Correspondence to:
Xiaoming Cai, email: [email protected]
Gang Feng, email: [email protected]
Keywords: SATB1, esophageal cancer, FN1, PDGFRB
Received: June 20, 2016 Accepted: January 16, 2017 Published: January 27, 2017
ABSTRACT
Esophageal cancer is a highly aggressive malignancy with very poor overall prognosis. Given the strong clinical relevance of SATB1 in esophagus cancer and other cancers suggested by previous studies, the exact function of SATB1 in esophagus cancer development is still unknown. Here we showed that the knockdown of SATB1 in esophageal cancer cell lines diminished the cell proliferation, survival and invasion. Whole genome transcriptome analysis of SATB1 knockdown cells revealed the different gene expression profiles between TE-1 cells and MDA-MB-231 cells. Network analysis and functional experiments further identified FN1 and PDGFRB to be key downstream genes regulated by SATB1 in esophageal cancer cells. Importantly, FN1 and PDGFRB were found to be highly expressed in human esophageal cancer. In summary, we provided the first molecular evidence that SATB1 played an oncogenic role in esophageal cancer by up-regulation of FN1 and PDGFRB.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 14849