Figure 2: Hypothetical cross talks between probiotics and multiple cell signaling pathways in colon carcinogenesis. Probiotics therapeutically intervene this cross talk with metabolites such as SCFA (butyrate) and CLA. PPARγ could be upregulated by CLA, which induces β-catenin for degradation hence controlled cellular proliferation by Wnt signaling inhibition; while in colon cancer condition, PPARγ is downregulated due to β-catenin mediated trans-deactivation appears to form loops (?) which needs to explore. Both butyrate and CLA could be able to modulate LOX and COX balance. HDACi activity of butyrate inhibit PI3/Akt pathway and indirectly it helps in the upregulation of PPARγ. Upregulated PPARγ inactivates NF-κB and activates pro-apoptotic signals while in another side PPARγ inhibit COX-2 which leads to downregulate the anti-apoptotic signals. Ultimately all these events (probiotics intervention) lead to inhibition of extensive cell proliferation of colonocytes, hence mitigation/reduction/elimination of colon cancer.