Background: Colon cancer is the most common type of gastrointestinal cancer. Despite advances
during the last two decades, the efficacy of colorectal cancer treatment is still insufficient and new anticancer
agents are necessary.
Methods: In our study, colon cancer cells derived from a primary tumor (SW480) and lymph node metastasis
(SW620) from the same patient were used and compared. The effect of flubendazole (FLU) on cell adhesion and
migration was monitored using the x-CELLigence Real-Time Cell Analysis system. Expressions of molecules involved
in adhesion and migration were analyzed using RT-PCR and western blot. Furthermore, RNA silencing of
nuclear factor-κB in SW620 cells was used to determine the involvement of the NF-κB p65 regulation pathway
in FLU action.
Results: FLU significantly suppressed the adhesion of SW480 cells and reduced the expression of adhesion
markers (ICAM-1, αE-catenin; β-catenin; integrin α5 and β1). Moreover, a significant anti-migratory potential
of FLU was manifested in the SW620 cells. In addition, FLU suppressed the phosphorylation of NF-κB p65 and
potentiated the suppression of several metastatic markers (ICAM-1, EpCAM, integrin α5, β1, α-tubulin) caused
by NF-κB p65 silencing.
Conclusion: FLU has a significant anti-migratory effect in intestinal cancer cell SW480 and its lymph node
metastatic cells SW620. FLU decreases the expression of some proteins involved in metastatic processes and
inhibits activation of NF-κB p65.