Regulatory Effect of CCL26 on Cancer Related Genes during Inflammation

Eotaxin‐3 (CCL26) is a member of the CC Chemokine family, which has been reported to have important roles in regulating cytokine release and expression during asthmatic inflammation. Eotaxin family has also been reported to be involved in tumor development and metastasis and cell proliferation. Such multiple bioactivities probably result from ability of eotaxins to modulate gene expression, protein synthesis, release and modification. This study focuses on the regulatory effect of CCL26 on the expression of cancer related genes and proteins during airway inflammation. 1 × 10 6 /well A549 were treated with 30 ng/ml interleukin 4 (IL‐4) plus or minus CCL26 for 24 hrs. Cell lysates were prepared and expression of genes and proteins was determined by Western Blot and Polymerase Chain Reaction (PCR). CCL26 increased the constitutive expression of Cathepsin B and Cyclin‐dependent Kinase 4 (Cdk4) to about 30% from control while decreasing Bok, JunB, MDM2, oncogene, and c‐Jun. Expressions of BTG2, Cyclin G1, ras homolog gene family member B (RhoB), Cdk 4, and Bok genes were increased during IL4 dependent inflammation, with the increase ranging from 5–44 % from control. On the contrary expressions of c‐Jun, JunB, and p53 were reduced. In the presence of IL‐4, CCL26 increased the expression of c‐Jun and Retinoblastoma (Rb) while reducing that of Heme Oxygenase, RhoB, and Bok with the highest increase and decrease of up to 400 and 54% for c‐Jun and Bok, respectively. These results suggest the involvement of CCL26 in regulating expression of cancer related genes during airway inflammation.