CCR10/CCL27 crosstalk regulates cell metastasis via PI3K-Akt signaling axis in non-small-cell lung cancer

Previous research has shown that CCR10 acts as a vital oncogene in the progression of multiple malignancies. However, its effect on the treatment of non-small-cell lung cancer (NSCLC) has not been investigated. Current research examined the effect of CCR10 on the cellular survival and migration of NSCLC, and the modulation of cell death and found that the expression levels of CCR10 and CCL27 (ligand) were highly upregulated in human NSCLC tissue and cell lines, A549 and H157, compared with adjacent normal lung specimens. MTT and colony formation assays revealed that the blockage of CCR10 inhibited the multiplication and survival of A549 and H157 cells. Further study showed that metastasis-relevant VEGF-C/D, M MP-2/9, TIM P-1/2 were also regulated via CCR10 activation. Notably, increased NF-kappa B levels were detected in cells with activated CCR10, whereas the levels of NF-kappa B decreased in cells with blocked CCR10. Finally, the recovery of NF-kappa B expression counteracted the suppressive influence of CCR10 blockage on NSCLC cell survival, migration, and invasion. These results improved our knowledge understanding the molecular mechanisms of CCR10-CCL27 in progression of NSCLC.