Next Article in Journal
TiO2 Immobilized on Manihot Carbon: Optimal Preparation and Evaluation of Its Activity in the Decomposition of Indigo Carmine
Previous Article in Journal
Rapid and Sensitive Identification of the Herbal Tea Ingredient Taraxacum formosanum Using Loop-Mediated Isothermal Amplification
Article Menu
Issue 1 (January) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2015, 16(1), 1576-1589; doi:10.3390/ijms16011576

Ponicidin Induces Apoptosis via JAK2 and STAT3 Signaling Pathways in Gastric Carcinoma

Department of Gastroenterology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, China
*
Author to whom correspondence should be addressed.
Academic Editor: Terrence Piva
Received: 23 September 2014 / Accepted: 18 December 2014 / Published: 12 January 2015
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
View Full-Text   |   Download PDF [3031 KB, uploaded 12 January 2015]   |  

Abstract

Ponicidin has a variety of biological effects such as immunoregulatory and anti-inflammatory functions as well as anti-viral functions especially in the upper respiratory tract infection. This study was aimed to elucidate the antitumor effect of ponicidin in gastric carcinoma MKN28 cells and the possible molecular mechanism involved. Cell viability was measured by the Cell Count Kit-8 (CCK8). Cell apoptosis was assessed by flow cytometry as well as cell cycle and reactive oxygen species (ROS) analysis. Western blot analysis was used to detect the active form of caspase-3 as well as Bax and B-cell lymphoma-2 (Bcl-2) expressions after cells were treated with different concentrations of ponicidin. The results revealed that ponicidin could inhibit the growth of MKN28 cells significantly in both a time- and dose-dependent manner. The cell cycle was blocked and ROS generation was increased after the cells were treated with ponicidin. Bcl-2 expression was down-regulated remarkably while Bax expression and the active form of caspase-3 were increased after apoptosis occurred. We therefore conclude that ponicidin exhibited significant growth inhibition of gastric carcinoma cell line MKN28 and induced apoptosis of MKN28 cells via the signaling pathway regulated by Janus kinase 2 (JAK2) and signal transducers and activators of transcription 3 (STAT3). Ponicidin may serve as a potential therapeutic agent for gastric carcinoma. View Full-Text
Keywords: ponicidin; gastric carcinoma; MKN28 cells; apoptosis; JAK2; STAT3 ponicidin; gastric carcinoma; MKN28 cells; apoptosis; JAK2; STAT3
Figures

Figure 1

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).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Liu, Y.-F.; Lu, Y.-M.; Qu, G.-Q.; Liu, Y.; Chen, W.-X.; Liao, X.-H.; Kong, W.-M. Ponicidin Induces Apoptosis via JAK2 and STAT3 Signaling Pathways in Gastric Carcinoma. Int. J. Mol. Sci. 2015, 16, 1576-1589.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[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