Affordable Access

Access to the full text

GATA1 promotes colorectal cancer cell proliferation, migration and invasion via activating AKT signaling pathway

Authors
  • Yu, Junhui1
  • Liu, Ming2
  • Liu, Hui3
  • Zhou, Lei4
  • 1 Capital Medical University, Department of Peritoneal Cancer Surgery, Beijing Shijitan Hospital, Beijing, 100038, People’s Republic of China , Beijing (China)
  • 2 Beijing Zhanlanlu Hospital, Department of Surgery, Beijing, 100044, People’s Republic of China , Beijing (China)
  • 3 Beijing University of Chinese Medicine, Department of Oncology, Huguosi Hospital of Traditional Chinese Medicine, Beijing, 100035, People’s Republic of China , Beijing (China)
  • 4 Capital Medical University, Department of Oncology, Beijing Shijitan Hospital, No 10 Tieyi Road, Yangfangdian Street, Haidian District, Beijing, 100038, People’s Republic of China , Beijing (China)
Type
Published Article
Journal
Molecular and Cellular Biochemistry
Publisher
Springer-Verlag
Publication Date
May 09, 2019
Volume
457
Issue
1-2
Pages
191–199
Identifiers
DOI: 10.1007/s11010-019-03523-w
Source
Springer Nature
Keywords
License
Yellow

Abstract

GATA1, a member of the GATA transcription factor family, was reported to play a role in development and progression of erythroid cells and breast cancer cells. However, the role of GATA1 in colorectal cancer (CRC) is unknown. Here, we demonstrate that GATA1 was upregulated in CRC tissues compared with normal tissues, and predicted poor clinical outcome in CRC. Biological functional analyses showed that GATA1 knockdown decreased CRC cells proliferation, migration and invasion, and regulated the process of epithelial–mesenchymal transition (EMT). Moreover, silencing of GATA1 suppressed colorectal tumor growth in nude mice. Mechanistically, GATA1 overexpression significantly increased the activity of PI3K/AKT signaling pathway in CRC cells. These data provide insight into the important role of GATA1 in CRC progression and suggest that GATA1 is a potential therapeutic target for CRC.

Report this publication

Statistics

Seen <100 times