We have demonstrated that BO 1051 induced apoptosis in HA22T/VGH and Mahlavu cells through a DNA damage signaling pathway. Upon inhibition of ATM or Decitabine structure, the apoptotic populace was considerably paid off. While BO1051 triggered clear apoptosis at the time level of 48 h after treatment, autophagy was seen when 8 h after BO 1051 was added to the culture medium. The readiness of LC3 II indicated that the induction of autophagy was time dependent, because it increased gradually until cells showed obvious signs of apoptosis. Nonetheless, the role of autophagy remains controversial: it’s been reported to be either prodeath or prosurvival. In HCC cell lines, autophagy can be induced by various compounds and can be involved in cell death or cytoprotection, as suggested previously. We for that reason chose an autophagy chemical, BafA1, to analyze the function of autophagy in BO 1051 induced cell death. Our data revealed that inhibitor could not prevent, but rather improved, BO 1051 induced cell death. Similarly, knockdown of Beclin 1 utilizing a particular shRNA showed the same result. We observed that inhibition of autophagy leads to increased apoptosis in both early or late stages inside our experiments, though it has been reported that inhibition of autophagy at different stages has other effects on cell survival. In effect, autophagy might have a Metastasis role in BO 1051 induced cell death, and is not strictly a prodeath device. The main reason that autophagy could be involved in cytoprotection could be defined with the studies using methylpyruvate, which acts as an energy source. Cells with useful autophagy have the ability to recycle and degrade cellular constituents and supply metabolic substrates for keeping the dynamic status. After DNA damage, autophagy may help to preserve the ATP concentration and thus delay the onset of apoptotic cell death. The function of ATM in cell death due to DNA damage is well defined. Nevertheless, ATM was recently found to be engaged in metabolic pathways apart from DNA damage. In addition, it has been noted that the knockout of ATM prevents the induction of autophagy in response CAL-101 PI3K inhibitor to ROS in human lymphoblast cells. Even though genotoxic stress is effective at inducing autophagy, direct evidence is still limited. Our results showed that the ATM kinase inhibitor, along with BO 1051 therapy, directly affects LC3 II conversion and p62/SQSTM1 destruction. Nevertheless, the effects of the ATM kinase chemical were opposite to the outcome obtained using siRNA to specifically knockdown ATM. While the ATM kinase chemical triggered autophagic flux, ATM knockdown had no effects on LC3 II or p62/SQSTM1 expression. Along side it aftereffects of the ATM kinase chemical might contribute these conflicting results.