Misc.

Peer-reviewed Last author Corresponding author
Jan, 2017

Anticancer effects of novel thalidomide analogs in A549 cells through inhibition of vascular endothelial growth factor and matrix metalloproteinase-2

BIOMEDICINE & PHARMACOTHERAPY
  • Bishoy El-Aarag
  • ,
  • Tomonari Kasai
  • ,
  • Junko Masuda
  • ,
  • Hussein Agwa
  • ,
  • Magdy Zahran
  • ,
  • Masaharu Seno

Volume
85
Number
First page
549
Last page
555
Language
English
Publishing type
DOI
10.1016/j.biopha.2016.11.063
Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER

Lung cancer is one of the major causes of cancer-related mortality worldwide, and non-small-cell lung cancer is the most common form of lung cancer. Several studies had shown that thalidomide has potential for prevention and therapy of cancer. Therefore, the current study aimed to investigate the antitumor effects of two novel thalidomide analogs in human lung cancer A549 cells. The antiproliferative, antimigratory, and apoptotic effects in A549 cells induced by thalidomide analogs were examined. In addition, their effects on the expression of mRNAs encoding vascular endothelial growth factor165 (VEGF165) and matrix metalloproteinase-2 (MMP-2) were evaluated. Their influence on the tumor volume in nude mice was also determined. Results revealed that thalidomide analogs exhibited antiproliferative, antimigratory, and apoptotic activities with more pronounced effect than thalidomide drug. Furthermore, analogs 1 and 2 suppressed the expression levels of VEGF165 by 42% and 53.2% and those of MMP-2 by 45% and 52%, respectively. Thalidomide analogs 1 and 2 also reduced the tumor volume by 30.11% and 53.52%, respectively. Therefore, this study provides evidence that thalidomide analogs may serve as a new therapeutic option for treating lung cancer. (C) 2016 Elsevier Masson SAS. All rights reserved.

Link information
DOI
https://doi.org/10.1016/j.biopha.2016.11.063
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000395522800064&DestApp=WOS_CPL
ID information
  • DOI : 10.1016/j.biopha.2016.11.063
  • ISSN : 0753-3322
  • eISSN : 1950-6007
  • Web of Science ID : WOS:000395522800064

Export
BibTeX RIS