Toll-like receptor 9 (TLR9) has been shown to have a significant role in
cancer.
MicroRNAs (
miRNAs), a group of small non-coding RNAs that fine tune translation of multiple target mRNAs, are involved in the development and progression of human
cancers. The present study was undertaken to determine the roles of TLR9 on
lung cancer and whether miR-26a is involved in TLR9‑mediated
lung cancer growth and migration. The
lung cancer models were elicited by injecting human
lung cancer cells into the left ventricle. The expression of TLR9 and miR-26a in
lung cancer tissues obtained from
lung cancer patients was increased. TLR9
ligand CpG-
oligodeoxynucleotides (
CpG-ODN) caused an increase in the mean
tumor weight and the size of
tumor mass in nude mice, and the proliferation and migration of H460 human
lung cancer cells.
CpG-ODN also induced an increase in the expression of miR-26a in H460 cells. The overexpression of miR-26a increased the weight and size of the
tumor mass in the nude mice, and the proliferation and migration of H460 cells. Expression of
phosphoinositide 3 kinase (PI3K) and phosphorylation of
protein kinase B (Akt) was increased after miR-26a overexpression in the H460 cells. PI3K inhibitor
wortmannin (WM) or Akt inhibitor
triciribine hydrate (TCN) eliminated the increase in the proliferation and migration induced by the overexpression of miR-26a in H460 cells. These results suggested that miR-26a is involved in the TLR9‑mediated growth and migration of
lung cancer through the PI3K-Akt signaling pathway.