Chronic exposure to particulate chromate induces spindle assembly checkpoint bypass in human lung cells.

摘要: One of the hallmarks lung cancer is chromosome instability (CIN), particularly a tetraploid phenotype, which normally prevented by spindle assembly checkpoint. Hexavalent chromium Cr(VI) an established human carcinogen, and induces tumors at bifurcation sites where particles impact persist. However, effects on checkpoint are unknown little known about prolonged exposure to particulate Cr(VI). Accordingly, we investigated Cr(VI)-induced bypass after several days in WHTBF-6 cells. We found that lead chromate indeed cells, as 72, 96, 120 h treatments with 0.5 or 1 microg/cm2 induced significant increases percentage cells aberrant mitotic figures. For example, treatment for 96 11, 12.3, 14% premature anaphase, centromere spreading division, respectively. In addition, disruption mitosis more accumulating anaphase; treated increased from 18% controls 31% chromate. To confirm involvement checkpoint, Mad2 expression was used marker. decreased exposed chronic chromate, consistent also concentration- time-dependent continued grow form colonies. When were alone there no increase polyploidy; however, soluble showed polyploidy. These data suggest does induce CIN may be one mechanism development cancer.