Several types of catenins work with N-cadherins to play an important role in learning and memory.
While less attention is directed at α-catenin in studies involving cell adhesion, it is nonetheless an important player in cellular organization, function and growth. α-catenin participates in the formation and stabilization of adherens junctions by binding to β-catenin-cadherin complexes in the cell. The exact protein dynamics by which α-catenin acts in adherens junctions is still unclear. It is believed however that α-catenin acts in concert with vinculin to bind to actin and stabilize the junctions.
As previously mentioned, the same properties of catenin that give it an important role in normal cell fate determination, homeostasis and growth, also make it susceptible to alterations that can lead to abnormal cell behavior and growth. Any changes in cytoskeletal organization and adhesion can lead to altered signaling, migration and a loss of contact inhibition that can promote cancer development and tumor formation. In particular, catenins have been identified to be major players in aberrant epithelial cell layer growth associated with various types of cancer. Mutations in genes encoding these proteins can lead to inactivation of cadherin cell adhesions and elimination of contact inhibition, allowing cells to proliferate and migrate, thus promoting tumorigenesis and cancer development. Catenins are known to be associated with colorectal and ovarian cancer, and they have been identified in pilomatrixoma, medulloblastoma, pleomorphic adenomas, and malignant mesothelioma.
While less is known about the exact mechanism of α-catenin, its presence in cancer is widely felt. Through the interaction of β-catenin and α-catenin, actin and E-cadherin are linked, providing the cell with a means of stable cell adhesion. However, decreases in this adhesion ability of the cell has been linked to metastasis and tumor progression. In normal cells, α-catenin may act as a tumor suppressor and can help prevent the adhesion defects associated with cancer. On the other hand, a lack of α-catenin can promote aberrant transcription, which can lead to cancer. As a result, it can be concluded, that cancers are most often associated with decreased levels of α-catenin.
β-catenin also likely plays a significant role in various forms of cancer development. However, in contrast to α-catenin, heightened β-catenin levels may be associated with carcinogenesis. In particular, abnormal interactions between epithelial cells and the extracellular matrix are associated with the over-expression of these β-catenins and their relationship with cadherins in some cancers. Stimulation of the Wnt/β-catenin pathway, and its role in promoting malignant tumor formations and metastases, has also been implicated in cancers.
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.
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 immunochemotherapy 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 in treating a variety of cancers.
While recent studies in the lab and in the clinic have provided promising results for treating various catenin-associated cancers, the Wnt/β-catenin pathway may make finding a single correct therapeutic target difficult as the pathway has been shown to elicit a variety of different actions and functions, some of which may possibly even prove to be anti-oncogenic.
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