Pei X H, Nakanishi Y, Takayama K, Yatsunami J, Bai F, Kawasaki M, Wakamatsu K, Tsuruta N, Mizuno K, Hara N
Research Institute for Diseases of the Chest, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Clin Exp Metastasis. 1996 Sep;14(4):351-7. doi: 10.1007/BF00123394.
The effects of exogenous and endogenous granulocyte colony-stimulating factor (G-CSF) on invasion by cancer cells were studied, using lung cancer cell lines that produce G-CSF (NCI-H157) and lines that do not (PC-9 and NCI-H23). The invasive capacity of NCI-H157 cells was 26- to 27-fold higher than that of PC-9 and NCI-H23 cells. The invasiveness of PC-9 cells was stimulated by exogenous G-CSF, while that of NCI-H157 cells was not. Antibodies against G-CSF blocked the stimulation of PC-9 cell invasiveness by exogenous G-CSF. Anti G-CSF antibodies also inhibited invasion by NCI-H157 cells in the absence of exogenous G-CSF. These results suggest that endogenous and exogenous G-CSF both stimulate invasion by lung cancer cells.
利用产生粒细胞集落刺激因子(G-CSF)的肺癌细胞系(NCI-H157)和不产生该因子的细胞系(PC-9和NCI-H23),研究了外源性和内源性G-CSF对癌细胞侵袭的影响。NCI-H157细胞的侵袭能力比PC-9和NCI-H23细胞高26至27倍。外源性G-CSF可刺激PC-9细胞的侵袭性,而对NCI-H157细胞则无此作用。抗G-CSF抗体可阻断外源性G-CSF对PC-9细胞侵袭性的刺激。在无外源性G-CSF的情况下,抗G-CSF抗体也可抑制NCI-H157细胞的侵袭。这些结果表明,内源性和外源性G-CSF均可刺激肺癌细胞的侵袭。