C-MYC is overexpressed in many types of
cancer linked to poor prognosis. We examined the c-Myc
protein expression in
adrenocortical cancer (ACC) cells to investigate the role of this
protein in the
neoplasm, its involvement in
chemotherapy and finally to determine whether c-Myc could be considered a prognostic factor in patients with ACC. H295R and SW13 cell lines were treated with
paclitaxel. c-Myc overexpressing cell clones were achieved by transfecting the H295R cell line with the pcDNA3-hMYC plasmid expressing the full-lengh C-MYC coding sequence. The SW13 cell line was transfected with
siRNA oligonucleotides for C-MYC. Cell cycle analysis was evaluated by flow cytometry. c-Myc,
cyclin B1 and pro
caspase expression levels were evaluated by western blot analysis. We found that expression of c-Myc was highly expressed in the SW13 cells, whereas the
protein was undetectable in the H295R cells. Different doses of
paclitaxel were required in the two ACC cell line to induce a block in the G2 phase, characterized by increased
cyclin B1 levels and to induce apoptosis by
pro-caspase-3 activation. Interestingly, the silencing of C-MYC
mRNA prevented
paclitaxel induced apoptosis in SW13 cells, whereas in the H295R cells the overexpression of C-MYC rendered the cells more prone to growth inhibition after
paclitaxel exposure. The present study directly demonstrates that C-MYC plays a central role in controlling proliferation in ACC cells after
paclitaxel treatment and that c-Myc could be considered as a marker for predicting response to chemotherapeutic agents in ACC cell lines.