The introduced cytoplasmic b catenin remains put through GSK 3b mediated phosphorylaton pan HSP90 inhibitor and destruction, when E cadherin is downregulated at EMT. Therefore, additional activation of the Akt pathway is necessary to prevent this method and facilitates the nuclear translocation and activation of b catenin. This speculation is consistent with the proven fact that EMT also correlates with the presence of w catenin in the nucleus. Ergo, activation of t catenin and Akt pathways is just a complete function at EMT and is important for generating highgrade invasive cells with stem cell like characteristics. Next, our suggest that targeting the b catenin and Akt pathways can suppress the stem cell like qualities associated with EMT. CSCs are often resistant to popular drugs in vivo and in vitro when compared with the majority of the cancer cell citizenry, raising the question of whether conventional treatment just debulks cancers, making CSCs to repopulate the initial tumor and which Lymphatic system in disease recurrence. Consistent with these findings, Cheng and her colleagues showed that the rest of the breast tumor cell populations that survived after conventional treatment were enriched for the subpopulation of cells with equally tumor stem cell like EMT traits and features. Thus, more effective solutions will need the selective targeting of the crucial cell population. The elucidation of molecular pathways underlying the regulation of CSC self-renewal and survival is vital for the success of this goal. Within our study, we found that both the knockdown of b catenin expression or the suppression of the Akt pathway by wortmannin inhibited CD44 expression. More over, the combination of both chemical withdrawal and siRNA knockdown considerably suppressed the expression of CD44, revealing the synergistic effect of those two pathways in maintaining the stem-cell like qualities connected with EMT. Gupta et al. recently applied a chemical screen and found compounds showing selective toxicity for breast CSCs, including Crizotinib c-Met inhibitor salinomycin. It’d be interesting to test whether Salinomycin prevents the activation of t catenin and Akt pathways in the forseeable future. Conclusion To sum up, we showed that the service of b catenin and Akt is important for the maintenance of CD44 expression associated with EMT. Targeting these pathways, in conjunction with currently used typical treatments, may supply a new therapeutic technique for reducing surviving tumor cells to prevent recurrence and to enhance longterm survival in cancer patients. Prostate apoptosis result protein 4 sensitizes cells to chemotherapy, however, Akt1 inactivates Par 4. Formerly we confirmed that Par 4 overexpressing a cancerous colon cells responded more quickly to 5 FU than did wild-type counterparts. In this review we investigated: 1) the effects of the Akt inhibitor, phenylbutyl isoselenocyanate, on tumor growth in nude mice and 2) by-stander effect of Par 4 overexpressing cells on wild type tumor growth.