can cause α-catenin to move from its normal location on the membrane into the nucleus and E-cadherin expression to decrease, thus promoting EMT and tumor invasiveness. There are other physiological factors that are associated with cancer development through their interactions with catenins. For instance, higher levels of collagen XXIII have been associated with higher levels of catenins in cells. These heightened levels of collagen helped facilitate adhesions and anchorage-independent cell growth and provided evidence of collagen XXIII's role in mediating metastasis. In another example, Wnt/β-catenin signaling has been identified as activating microRNA-181s in hepatocellular carcinoma that play a role in its tumorigenesis. Recent clinical studies Recently, there have been a number of studies in the lab and in the clinic investigating new possible therapies for cancers associated with catenin. Integrin antagonists and immonochemotherapy with 5-fluorouracil plus polysaccharide-K have shown promising results. Polysaccharide K can promote apoptosis by inhibiting NF-κB activation, which is normally up-regulated, and inhibiting apoptosis, when β-catenin levels are increased in cancer. Therefore, using polysaccharide K to inhibit NF-κB activation can be used to treat patients with high β-catenin levels. In the short-term, combining current treatment techniques with therapeutics targeting catenin-associated elements of cancer might be most effective in treating the disease. By disrupting Wnt/β-catenin signaling pathways, short-term neoadjuvant radiotherapy (STNR) may help prevent clinical recurrence of the disease after surgery, but much more work is needed before an adequate treatment based on this concept can be determined. Lab studies have also implicated potential therapeutic targets for future clinical studies. VEGFR-1 and EMT mediators may be ideal targets for preventing cancer development and metastasis. 5-aminosalicylate (ASA) has been shown to reduce β-catenin and its localization to the nucleus in colon cancer cells isolated from and in patients. As a result, it may be useful as a chemopreventative agent for colorectal cancer. Additionally, acyl hydrazones have been shown to inhibit the Wnt signaling characteristic of many cancers by destabilizing β-catenin, thus disrupting Wnt signaling and preventing the aberrant cell growth associated with cancer. On the other hand, some treatment concepts involve upregulating the E-cadherin/catenin adhesion system to prevent disruptions in adhesions and contact inhibition from promoting cancer metastasis. One possible way to achieve this, which has been successful in mouse models, is to use inhibitors of Ras activation in order to enhance the functionality of these adhesion systems. Other catenin, cadherin or cell cycle regulators may also be useful