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World J Gastroenterol. Mar 21, 2014; 20(11): 2979-2994
Published online Mar 21, 2014. doi: 10.3748/wjg.v20.i11.2979
Published online Mar 21, 2014. doi: 10.3748/wjg.v20.i11.2979
Differential gene expression of chemokines in KRAS and BRAF mutated colorectal cell lines: Role of cytokines
Sajjad Khan, Silke Cameron, Martina Blaschke, Federico Moriconi, Naila Naz, Ahmad Amanzada, Giuliano Ramadori, Ihtzaz Ahmed Malik, Clinic of Gastroenterology and Endocrinology, University Medical Center, Robert-Koch-Str. 40, 37075 Goettingen, Germany
Author contributions: Khan S, Ramadori G and Malik IA defined the research theme; Khan S designed methods and experiments, carried out all the laboratory experiments, analyzed the data, interpreted the results and wrote the paper; Cameron S and Blaschke M co-worked on associated data collection and their interpretation; Naz N, Moriconi F and Amanzada A co-designed experiments, discussed analyses, interpretation, and presentation; all authors have contributed to, seen and approved the manuscript.
Supported by The German Research Foundation and the Open Access Publication Funds of the Göttingen University
Correspondence to: Dr. Ihtzaz Ahmed Malik, Clinic of Gastroenterology and Endocrinology, University Medical Center, Robert-Koch-Str. 40, 37075 Goettingen, Germany. i.malik@med.uni-goettingen.de
Telephone: +49-551-398902 Fax: +49-551-399820
Received: August 21, 2013
Revised: December 5, 2013
Accepted: January 2, 2014
Published online: March 21, 2014
Revised: December 5, 2013
Accepted: January 2, 2014
Published online: March 21, 2014
Core Tip
Core tip: The presence of KRAS/BRAF mutations in advanced colorectal-cancer influences the efficacy of treatment. It is not known whether the composition of tumor-associated immune cells is influenced by the mutational status of the tumor. The results of our study show a higher expression of pro-angiogenic chemokines at basal level in mutated cell-lines, which was further up-regulated by cytokine treatment. Moreover, specific KRAS inhibition resulted in an increase of pro-angiogenic chemokines, mainly through the NF-κB pathway in wt (Caco2). Our findings point to the interconnection of tumor mutation and its microenvironment.