(1) Background: Epithelial ovarian cancer (EOC) is the most lethal cancer of the female reproductive system. In an earlier study, we identified multiple genes as hypermethylated in tumors of patients with poor prognosis. The most promising combination of markers to predict a patient’s outcome was
CaMKIINα and
RUNX3. Aim of this study was to functionally validate the importance of both genes. (2) Methods: IC
50 measurements, cell cycle distribution-, proliferation, and migration experiments were conducted after transgene overexpression in two EOC cell lines. (3) Results: We showed that
CaMKIINα has tumor suppressive functions in vitro and reduces proliferation, migration, and colony formation. However, it had no effect on the reversion of the resistance to cisplatin.
RUNX3 exhibited dualistic functions related to cisplatin sensitivity and migration capacity, depending on the respective transcript variant (TV). A2780 cells expressing
RUNX3 TV2—the promoter of which harbors a CpG (5′-C-phosphate-G-3′) island and is potentially inactivated by hypermethylation—exhibited increased cisplatin sensitivity and reduced migration properties. However,
RUNX3 TV1, not affected by CpG island methylation could be characterized as mediating resistance and enhancing migration in A2780. The higher resistance of
RUNX3 TV1 transfected cells correlates with a reduction of cell proliferation. Moreover,
RUNX3 TV1 expressing cells exhibit a reduced cell cycle arrest at the gap-2 or mitosis phase (G2/M) under cisplatin treatment comparable to resistant A2780 subcultures. (4) Conclusion: It appears that
CaMKIINα and
RUNX3 TV2 can reduce the malignant potential of EOC cells.
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