Inclusion of SCR7, a decline in the recombination, following normalization of transfection performance, was observed indicating inhibition of NHEJ at the intracellular level. Centered on the above findings, we wondered whether the inhibition of implicit NHEJ you could end up the accumulation of unrepaired DSBs in the genome level. To check this, we handled breast and cervical order Doxorubicin cancer cell lines with SCR7, followed by immunofluorescence and western blotting studies, by using anti gH2AX. Results showed a rise in levels of protein and gH2AX foci, indicative of unrepaired DSBs with-in cells. The number of foci seen on account of SCR7 was much like those generated during siRNA knockdown of Ligase IV. As a get a handle on, we employed scrambled siRNA and siRNA against Ligase I and III. But, similar studies on K562 cells did not produce any gH2AX foci, even at highest levels of SCR7, possibly Infectious causes of cancer because of low expression of Ligase IV. To exclude the possibility that SCR7 can make DSBs immediately, independent of N114, Ligase IV, and Nalm6 cells were treated with SCR7 and examined for gH2AX levels by western blotting and immunofluorescence. Results showed that gH2AX expression remained unchanged upon SCR7 treatment in Ligase IV / cells, while an important increase was noted in the event of Nalm6 cells. Both the cell lines showed large advancement in gH2AX and foci expression upon bleomycin treatment, a known DSB inducing agent. Overall, these results suggest that SCR7 doesn’t stimulate DSBs right to the genome and is Ligase I-V dependent. Besides, upon incubation of oligomeric dsDNA or supercoiled plasmid DNA with increasing levels of SCR7, there is no evidence for DNA breaks. Thus, SCR7 interferes with NHEJ in cells, ultimately causing accumulation of unrepaired DSBs. To gauge whether deposition of DSBs leads to cell death upon SCR7 treatment, we conducted an evaluation of cytotoxicity among various human angiogenic inhibitor cell lines based on breast, cervical, lung, and ovarian cancers, fibrosarcoma, and leukemia, through the use of both MTT or trypan blue exclusion assays. Results showed a dose-dependent decrease in cell proliferation of MCF7, A549, and HeLa having an IC50 of 44 mM, respectively, that was further confirmed by DIC imaging in MCF7. T47D, A2780, and HT1080 were also painful and sensitive to SCR7, with an IC50 of 10 mM, respectively. In contrast, SCR7mediated cytotoxicity was confined when leukemic cell lines were used, except for Nalm6, which showed an IC50 of 50 mM. Phrase of Ligase IV in various cancer cells might be linked with their sensitivity to SCR7, with an exception of T47D, which has low quantities of Ligase IV. This might be possibly due to a change within the proapoptotic to antiapoptotic proportion, because of its aberrant BCL2 position. To determine the effect e