In this study, the apoptotic effects of the actin disruption agent, latrunculin B(LB) have been investigated on p53 deficient chronic myeloid leukemia cell line K562. A dose-dependent decrease in K562 cell proliferation was observed after LB treatment with maximum decrease in cell proliferation being at 1.5μM where the percent inhibition was 66.53%. F-actin stained with TRITC-phalloidin was shown as a peripheral ring or appeared diffusely distributed throughout the cytoplasm in untreated cells, this actin ring was decreased following LB treatment, and even large focal actin aggregates were formed. Treatment of K562 with LB(1.5μM) generated ROS substantially. LB activated expression in a dose-dependent manner. Therefore it can be concluded that LB, depolymerising agent of actin, induces apoptosis by producing ROS and up-regulating NF-kB and COX-2 activation.

I. Introduction
 II. Materials and Methods
  1. Cell culture
  2. Chemicals
  3. Viability assay
  4. Immunocytochemistry
  5. Measurement of intracellular ROS
  6. Determination of Nitric Oxide(NO)
  7. Western blot analysis
  8. Fluorescence-activated cell sorter(FACS)
 III. Results
  1. LB inhibits the growth of hematopoieticcancer cell lines
  2. LB destabilizes actin filaments and inducesapoptosis
  3. ROS generated by LB, but not NO
  4. Effect of latrunculin B on cell cycle progression
  5. PARP-1 cleavage in response to LB treatment
  6. Latrunculin B activated NF-kB and COX-2
 IV. Discussion
 V. References

• 김지영(Department of Oral Pathology, School of Dentistry, Pusan National University) | Ji Young Kim
• 박혜련(Department of Oral Pathology, School of Dentistry, Pusan National University) | Hae Ryoun Park
• 안원근(Department of Oral Pathology, School of Dentistry, Pusan National University) | Won Gun An correspondence