s connected with apoptosis induction. The links between ERK initial, p21WAF1/CIP1 induction and Bcl 2 inhibition in reaction to the compound remain to be clarified. Zhu et a-l. Shown that inhibition of ERK phosphorylation by PD98059 or UO126 attenuated DCPE induced expression of p21WAF1/CIP1 in DLD 1 a cancerous colon cells. This can be in agreement with many reports arguing CTEP that ERK activation induces p21WAF1/CIP1 appearance in various cellular types. Particularly, stimulation of ERK in a reaction to cisplatin was demonstrated to up regulate p21WAF1/CIP1 stage in the A2780 ovarian carcinoma cell line. ERK path was also explained to indirectly regulate the expression of a few members of the Bcl 2 family protein, including Bcl xL, Mcl 1 and Bcl 2 it self, via NFKB activation. After gemcitabine treatment, ERK activation was reported to lead to Bcl 2 down regulation in non-small cell lung cancer cell lines. Conversely, Bcl 2 also can act upstream of ERK. Like, overexpression of Bcl 2 suppressed cisplatin induced Organism activation of ERK in rat neuroblastoma cells. But, our results provided ERK initial, information, p21WAF1/CIP1 induction and down-regulation of Bcl 2 being related or-not, depending on the considered cell line. For example, whereas ERK activation and p21WAF1/CIP1 induction seemed to be related in R and OAW42 cell lines, these events were clearly in-dependent within the IGROV1 R10 cell line. We’d previously demonstrated that progressive order of resistance by OAW42 Dtc cells was of a progressive loss of ERK activation in response to cisplatin. The capability of DCPE to cause ERK activation within the OAW42 Kiminas cell line incited us to explore its influence on cisplatininduced apoptosis in this resistant ovarian carcinoma design which lacked P ERK. There is conflicting evidence for the role of P ERK in influencing MAPK signaling survival of cells treated with cisplatin. Whereas some writers have suggested that P ERK may be associated with chemoresistance, in particular in ovarian carcinoma cell lines, many studies demonstrated an association between ERK activation and sensitivity to the cytotoxic agent. Hence, Wang et a-l. confirmed that, in a cancer cell line, resistant options displayed paid off activation of ERK following cisplatin therapy. Furthermore, inhibition of MEK/ERK pathway generated cisplatin resistance in various cancer mobile types, while cisplatin induced apoptosis was increased by transient transfection of constitutively active MEK1. In this study, we showed the combined therapy with cisplatin and DCPE was more efficient to induce apoptosis in OAW42 Page1=46 cells than administration of each of those agents alone. In addition to its anticancer properties, DCPE hence appeared as a efficient