The type 1
insulin-like growth factor receptor (IGF-1R) and its
downstream signaling components have been increasingly recognized to
drive the development of
malignancies, including
non-small cell lung cancer (NSCLC). This study aimed to investigate the effects of IGF-1R and its inhibitor, AG1024, on the progression of
lung cancer.
Tissue microarray and
immunohistochemistry were employed to detect the expressions of
IGF-1 and IGF-1R in NSCLC
tissues (n=198).
Western blotting was used to determine the expressions of
IGF-1 and phosphorylated IGF-1R (p-IGF-1R) in A549
human lung carcinoma cells, and MTT assay to
measure cell proliferation. Additionally, the expressions of
IGF-1, p-IGF-1R and IGF-1R in a
mouse model of
lung cancer were detected by
Western blotting and real-
time fluorescence quantitative
polymerase chain reaction (FQ-
PCR), respectively. The results showed that
IGF-1 and IGF-1R were overexpressed in NSCLC
tissues. The expression levels of
IGF-1 and p-IGF-1R were significantly increased in
A549 cells treated with
IGF-1 as compared to those treated with
IGF-1+AG1024 or untreated
cells. In the presence of
IGF-1, the proliferation of
A549 cells was significantly increased. The progression of
lung cancer in
mice treated with
IGF-1 was significantly increased as compared to the group treated with
IGF-1+AG1024 or the
control group, with the same trend mirrored in
IGF-1/p-IGF-1R/IGF-1R at the
protein and/or
mRNA levels. It was concluded that
IGF-1 and IGF inhibitor AG1024 promotes
lung cancer progression.