Etoposide (VP-16) elicits apoptosis following prolonged G2-M cell arrest in p53-mutated human non-small cell lung cancer cells

The clinically important therapeutic agent VP-16-mediated prolonged cell arrest at G2-M phase prior to apoptotic death offered a different perspective in restraining human cancer cells at low drug dosage, thereby serving as an effective telomerase inhibitor as well as an apoptosis effector. The overall results demonstrated that apoptosis can be regulated differently in human NSCLC cells with disrupted p53. Further effort in elucidating G2-M arrest before leading to apoptosis promises to provide an alternative insight in reversing tumorigenic phenotype of human cancers.