Suzuki Eiji, Ota Tetsuya, Tsukuda Kazunori, Okita Atsushi, Matsuoka Kinya, Murakami Masakazu, Doihara Hiroyoshi, Shimizu Nobuyoshi
Department of Cancer and Thoracic Surgery, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan.
Int J Cancer. 2004 Jan 10;108(2):207-11. doi: 10.1002/ijc.11546.
The nm23-H1 gene is known as a potential metastasis suppressor gene in various types of carcinomas. However, the role of nm23-H1 in colorectal carcinoma still remains controversial and the cellular mechanisms by which its protein may modulate the metastatic phenotype are not yet known. We transfected nm23-H1 cDNA into the human colon cancer cell line, HT-29, to test the effects and cellular biological mechanism of nm23 protein in colon cancer. We found that nm23-H1 strongly inhibited the liver metastasis of HT-29 cells in nude mice and inhibited the epidermal growth factor (EGF)-induced cell migration in vitro. Furthermore, we clarified the regulation of the myosin light chain (MLC) phosphorylation by nm23-H1, which has been demonstrated as having potential role in cell migration.
nm23-H1基因在各类癌症中被认为是一种潜在的转移抑制基因。然而,nm23-H1在结直肠癌中的作用仍存在争议,其蛋白质调节转移表型的细胞机制尚不清楚。我们将nm23-H1 cDNA转染到人结肠癌细胞系HT-29中,以测试nm23蛋白在结肠癌中的作用及其细胞生物学机制。我们发现nm23-H1强烈抑制HT-29细胞在裸鼠中的肝转移,并在体外抑制表皮生长因子(EGF)诱导的细胞迁移。此外,我们阐明了nm23-H1对肌球蛋白轻链(MLC)磷酸化的调节作用,MLC磷酸化已被证明在细胞迁移中具有潜在作用。