Vitamin K3-induced cell cycle arrest and apoptotic cell death are accompanied by altered expression of c-fos and c-myc in nasopharyngeal carcinoma cells.
Vitamin K3 is known to inhibit the growth of various rodent and human tumor cells. However, the molecular mechanism of its action is still elusive. We have found that vitamin K3 induces cell cycle arrest and apoptotic cell death in nasopharyngeal carcinoma (NPC) cells, as evaluated by flow cytometry and DNA gel electrophoresis. Involvement of c-fos and c-myc proto-oncogenes and expression of their proto-oncoproteins in VK3-induced cell cycle arrest and apoptosis were also investigated. Northern blot analysis of NPC cells treated with 50 microM VK3 showed that c-fos was transiently induced for 60 min after treatment, while c-myc was persistently induced for 1-9 h after drug treatment. Western blot analysis also showed that c-Fos was induced at 4-6 h and at 1-4 h after treatment with 50 microM and 200 microM VK3 respectively, while c-Myc was induced at 1-6 h and at 4-6 h, respectively, after such treatments. These results suggest that the expression of c-fos and c-myc may play an important role in the signaling mechanism of VK3-induced growth arrest and apoptotic cell death.
Wu
F Y
FY
Cancer Research Group, Institute of Biomedical Sciences (IBMS), Academia Sinica, Taipei, Taiwan, Republic of China.
Chang
N T
NT
Chen
W J
WJ
Juan
C C
CC
D000199:Actins / Q000235:genetics; D017209:Apoptosis / Q000187:drug effects*; D002277:Carcinoma / Q000235:genetics* / Q000473:pathology; D002453:Cell Cycle / Q000187:drug effects; D004273:DNA, Neoplasm / Q000378:metabolism; D016762:Genes, fos; D016259:Genes, myc; D006801:Humans; D009303:Nasopharyngeal Neoplasms / Q000235:genetics* / Q000473:pathology; D014407:Tumor Cells, Cultured; D014812:Vitamin K / Q000494:pharmacology*
D000199:Actins; D004273:DNA, Neoplasm; D014812:Vitamin K