Human MCF-7 breast cancer cells have p53-wild type, yet it does not readily undergo p53-depedent apoptosis. As guardian of genome p53 is at the hub of numerous signalling pathways of baseline level DNA damage, by binding to spesific DNA sequences and transactivates a number of genes to lead into the transient cell cycle arrest or triggering apoptotic cell death. In addition to nuclear activity, p53 also possesses some cytosolic and transcription-independent activities that was also associated with apoptotic. Typhonium flagelliforme, more commonly known as Keladi Tikus in Indonesia, plays a role for the cell-cycle arrest or trigger for apoptosis. The aimed of study is having assessed the expression levels of p53, as well as cellular localization to investigate the correlation of apoptotic-dependent or independent p53 on the MCF-7 cells folloeing treatment. This study adapts laboratory experimental in-vitro in MCF-7 cells, with post test control group only design, and divided into two groups, were incubated in 10h and 20h. The control group received no other treatment. The treatment group received the tuber extract of Typhonium flagelliforme DCM fraction, in 62,08 g/mL (IC50) followed by Immunocytochemical analysis to observe the expression of p53. Sample T test shows a significant differences in treatment groups compared with the controls (p<0,01). There were increased in the expression of nuclear p53. The increasing of nuclear p53 plays a role in apoptotic on MCF-7 cells following treatment tuber extract of Typhonium flagelliforme DCM fraction. p53, MCF-7 cell, tuber extract of Typhonium flagelliforme DCM Fraction.