Oncotarget

Research Papers:

Ets2 knockdown inhibits tumorigenesis in esophageal squamous cell carcinoma in vivo and in vitro

Qinghua Li, Lu Yang, Kang Han, Liqiang Zhu, Yanting Zhang, Shanshan Ma, Kun Zhang, Bo Yang and Fangxia Guan _

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2016; 7:61458-61468. https://doi.org/10.18632/oncotarget.11369

Metrics: PDF 1532 views  |   HTML 1858 views  |   ?  


Abstract

Qinghua Li1,2,*, Lu Yang2,*, Kang Han2,*, Liqiang Zhu3, Yanting Zhang2, Shanshan Ma2, Kun Zhang2, Bo Yang1, Fangxia Guan1,2

1The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China

2School of Life Sciences, Zhengzhou University, Zhengzhou 450001, Henan Province, China

3The Second Affiliated Hospital of Zhengzhou University, Zhengzhou 450002, Henan Province, China

*These authors contributed equally to this work

Correspondence to:

Fangxia Guan, email: [email protected]

Bo Yang, email: [email protected]

Keywords: Ets2, esophageal squamous cell carcinoma, proliferation, apoptosis, mTOR/p70S6K signaling pathway

Received: December 10, 2015     Accepted: August 08, 2016     Published: August 18, 2016

ABSTRACT

Increased expression of Ets2 is reported upregulated in esophageal squamous cell carcinoma tissue. However, the function of Ets2 in carcinogenesis of ESCC is poorly understood. Here, the rise of Ets2 was confirmed in ESCC cells and Ets2 depletion by RNA interference promotes cell apoptosis, inhibits cell proliferation, attenuates cell invasion and induces cell cycle G0/G1 arrest in vitro. Moreover, in vivo, Xenograft mouse model studies showed Ets2 knockdown inhibits tumor formation and metastasis significantly. Furthermore, Ets2 depletion inactivates the mTOR/p70S6K signaling pathway both in vitro and in vivo. Taken together, these findings strongly suggest that a critical role of Ets2 in human ESCC pathogenesis via the inactivation of the mTOR/p70S6K signaling pathway.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 11369