we considered the therapeutic potential of a soluble Wnt receptor decoy in cancer gene therapy. We developed a Wnt antagonist sLRP6E1E2, and developed a replication inexperienced adenovirus, dE1 k35/sLRP6E1E2, and a replication qualified oncolytic Ad, RdB k35/ Lonafarnib 193275-84-2 sLRP6E1E2, both showing sLRP6E1E2. sLRP6E1E2 stopped Wnt mediated stabilization of cytoplasmic b catenin, reduced Wnt/b catenin signaling and cell growth via the mitogen activated protein kinase, and phosphatidylinositol 3 kinase pathways. sLRP6E1E2 caused apoptosis, cytochrome c release, and increased cleavage of caspase and PARP 3. sLRP6E1E2 suppressed growth of the human lung tumor xenograft, and reduced motility and invasion of cancer cells. In addition, sLRP6E1E2 up-regulated expression of epithelial marker genes, while sLRP6E1E2 downregulated mesenchymal marker genes. Taken together, sLRP6E1E2, by inhibiting conversation between Wnt and its receptor, suppressed Wnt stimulated cell Digestion growth and epithelial to mesenchymal transition. Lung cancer is very ambitious and the most frequent cause of cancer related deaths global. Last Year, the American Cancer Society estimated that there have been 219,440 new cases of lung cancer in america. Common therapies including surgery and radiation aren’t successful in several cases, however, a heightened understanding of the molecular mechanisms of lung cancer has resulted in the development of promising new therapies. Though chemotherapy developments have improved over all survival for patients with aggressive non-small cell lung cancer, chemoresistance remains a major cause of treatment failure. Several intense lung cancers show variations in a variety of cancerassociated genes, including cyclo-oxygenase 2, K ras, extra-cellular signalregulated Doxorubicin clinical trial kinase, Akt, and Wnt, suggesting another molecular pathway for carcinogenesis in lung adenocarcinomas. The function of Wnt signaling in cancer was suggested 20 years ago with the discovery of Wnt 1 being an integration site for mouse mammary tumor virus. Many studies have documented that altered expression of Wnt ligands, receptors, and extracellular antagonists are associated with cancer development/progression and stem cell self renewal/differentiation. Appearance of the Wnt ligand, low-density lipoprotein receptor related protein 5, and LRP6 are up-regulated in lung cancers, whereas Wnt antagonists that bind Wnt ligands to block interaction with receptors, produced Frizzled related proteins and dickkopf proteins are down-regulated or inactivated. Consequently, monoclonal antibodies and little interfering RNAs against Wnt and over-expression of Wnt antagonists reduce tumor growth in various in vitro and in vivo tumor models. LRP6, a part of the LRP superfamily, is necessary for service of the canonical Wnt signaling pathway, which leads to the stabilization and nuclear translocation of t catenin, the important thing effector molecule.