Next Article in Journal
Treating the Synapse in Major Psychiatric Disorders: The Role of Postsynaptic Density Network in Dopamine-Glutamate Interplay and Psychopharmacologic Drugs Molecular Actions
Next Article in Special Issue
Exploration of the Esophageal Mucosal Barrier in Non-Erosive Reflux Disease
Previous Article in Journal
Zinc as a Signal to Stimulate Red Blood Cell Formation in Fish
Article Menu
Issue 1 (January) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2017, 18(1), 134;

Shp2 Inhibits Proliferation of Esophageal Squamous Cell Cancer via Dephosphorylation of Stat3

1,* and 1,*
Department of Thoracic Surgery, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai 200003, China
Department of Oncology, Cancer Center, People’s Liberation Army General Hospital of Shenyang Military Region, Shenyang 110016, China
These authors contribute equally to this work.
Authors to whom correspondence should be addressed.
Academic Editor: Marco G. Patti
Received: 4 November 2016 / Revised: 21 December 2016 / Accepted: 4 January 2017 / Published: 12 January 2017
(This article belongs to the Special Issue Gastroesophageal Reflux Disease: It Is More than Just Heartburn)
Full-Text   |   PDF [3350 KB, uploaded 12 January 2017]   |  


Shp2 (Src-homology 2 domain-containing phosphatase 2) was originally reported as an oncogene in kinds of solid tumors and hematologic malignancies. However, recent studies indicated that Shp2 may act as tumor suppressors in several tumor types. We investigated the function of Shp2 in esophageal squamous cell cancer (ESCC). The expression level of Shp2 was analyzed in tumor tissues in comparison with adjacent normal tissues of ESCC patients by immunohistochemistry and Western blot. Shp2 was knocked down by Short hairpin RNA to evaluate its function in ESCC cell lines. The relationship between Shp2 and p-Stat3 (signal transducer and activator of transcription 3) in human ESCC tissues was statistically examined. A significant low expression of Shp2 was found in ESCC tissues. Low expression of Shp2 was related to poorer overall survival in patients from The Cancer Genome Atlas (TCGA) dataset. Knockdown of Shp2 increased the growth of ESCC cell lines both in vivo and vitro. Activation of Stat3 (p-Stat3) was induced by Shp2 depletion. Expression of p-Stat3 was negatively correlated with Shp2 expression in ESCC tissues. Furthermore, knockdown of Shp2 attenuated cisplatin-sensitivity of ESCC cells. Shp2 might suppress the proliferation of ESCC by dephosphorylation of p-Stat3 and represents a novel research field for targeted therapy. View Full-Text
Keywords: esophageal squamous cell cancer; proliferation; Shp2 esophageal squamous cell cancer; proliferation; Shp2

Figure 1a

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Supplementary material


Share & Cite This Article

MDPI and ACS Style

Qi, C.; Han, T.; Tang, H.; Huang, K.; Min, J.; Li, J.; Ding, X.; Xu, Z. Shp2 Inhibits Proliferation of Esophageal Squamous Cell Cancer via Dephosphorylation of Stat3. Int. J. Mol. Sci. 2017, 18, 134.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top