Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

Effect of CXCL12/CXCR4 on increasing the metastatic potential of non‑small cell lung cancer in vitro is inhibited through the downregulation of CXCR4 chemokine receptor expression

Effect of CXCL12/CXCR4 on increasing the metastatic potential of non‑small cell lung cancer in... Lung cancer ranks as the most common type of cancer in males worldwide. Although great advances have been achieved in chemotherapy and radiotherapy, the long‑term survival rate of lung cancer patients has not improved significantly. Dissemination of lung cancer in the thoracic cavity and metastatic spread to the liver, bone and brain are characteristic of non‑small cell lung cancer (NSCLC), constituting the primary source of morbidity and mortality in lung cancer. Increasing evidence also indicates that the CXC chemokine receptor 4 (CXCR4)/chemokine CXC motif ligand 12 (CXCL12) chemokine axis is important for the cell invasion and migration of lung cancer. CXCR4 is a G protein‑coupled receptor with a major role in lymphocyte homing. Its ligand, CXCL12, is secreted by target organs and functions as a highly efficient chemotactic factor for T cells, monocytes, pre‑B cells, dendritic cells and myeloid bone marrow‑derived cells. In the current study, recombinant CXCR4‑specific small interfering RNA‑pBSilence1.1 plasmids were constructed and transfected into the A549 NSCLC cell line in vitro. Reverse transcription polymerase chain reaction and western blotting revealed that CXCR4 was downregulated in transfected cells compared with control cells. The results of MTT and Transwell migration assays indicated that the specific downregulation of CXCR4 inhibited cell growth, invasiveness and migration. Thus, siRNA targeting of CXCR4 may effectively inhibit the effect of CXCL12/CXCR4 on increasing the metastatic potential of NSCLC. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Oncology Letters Spandidos Publications

Effect of CXCL12/CXCR4 on increasing the metastatic potential of non‑small cell lung cancer in vitro is inhibited through the downregulation of CXCR4 chemokine receptor expression

Download PDF
7 pages

Loading next page...
 
/lp/spandidos-publications/effect-of-cxcl12-cxcr4-on-increasing-the-metastatic-potential-of-non-WBldWwMvyA

References (29)

Publisher
Spandidos Publications
Copyright
Copyright © Spandidos Publications
ISSN
1792-1074
eISSN
1792-1082
DOI
10.3892/ol.2014.1837
Publisher site
See Article on Publisher Site

Abstract

Lung cancer ranks as the most common type of cancer in males worldwide. Although great advances have been achieved in chemotherapy and radiotherapy, the long‑term survival rate of lung cancer patients has not improved significantly. Dissemination of lung cancer in the thoracic cavity and metastatic spread to the liver, bone and brain are characteristic of non‑small cell lung cancer (NSCLC), constituting the primary source of morbidity and mortality in lung cancer. Increasing evidence also indicates that the CXC chemokine receptor 4 (CXCR4)/chemokine CXC motif ligand 12 (CXCL12) chemokine axis is important for the cell invasion and migration of lung cancer. CXCR4 is a G protein‑coupled receptor with a major role in lymphocyte homing. Its ligand, CXCL12, is secreted by target organs and functions as a highly efficient chemotactic factor for T cells, monocytes, pre‑B cells, dendritic cells and myeloid bone marrow‑derived cells. In the current study, recombinant CXCR4‑specific small interfering RNA‑pBSilence1.1 plasmids were constructed and transfected into the A549 NSCLC cell line in vitro. Reverse transcription polymerase chain reaction and western blotting revealed that CXCR4 was downregulated in transfected cells compared with control cells. The results of MTT and Transwell migration assays indicated that the specific downregulation of CXCR4 inhibited cell growth, invasiveness and migration. Thus, siRNA targeting of CXCR4 may effectively inhibit the effect of CXCL12/CXCR4 on increasing the metastatic potential of NSCLC.

Journal

Oncology Letters – Spandidos Publications

Published: Apr 1, 2014

There are no references for this article.