Latest rejection of pancreatic protein, pancreatic exocrine adenocarcinoma of the common visceral malignancy in the second place, is the cause of death in the American Cancer fifth disease, gastrointestinal cancer deaths accounted for 1 / 5. Because the pancreas is located in retroperitoneum, making it difficult to get early treatment, however, the recent development of this medical diagnosis and treatment of refractory disease continues to generate
Stanford University School of Medicine have discovered a new protein suppressed pancreatic cancer, blocking the expression of the protein can slow or stop tumor growth in mice, and to develop the cancer cells more susceptible to occur in hypoxic conditions in solid tumors effects. The findings are published in the February 1 issue of "Cancer Research" magazine.
Cancer experts called connective tissue growth factor (CTGF) protein CCN2 studied, the protein and the body to react to injury or disease, the abnormal growth of connective tissue, but also on pancreatic tumor growth may be related, but role is still unclear.
Researchers Garcia and his colleagues found that high levels of CCN2 values expressed as human pancreatic cancer cells were injected into mouse skin will quickly grow. In fact, a growing tumors, these cells will soon be expressed as those cells with low protein levels of competition. In contrast, CCN2 expression was suppressed in pancreatic cancer cells when injected into mice is neither possible nor the formation of tumors.
In pancreatic cancer cells were injected into animals, the researchers observed a similar effect. And expression of low levels of CCN2 in cancer cells compared to the high levels of CCN2 expression in cancer cells formed tumors more quickly, more positive shift. High levels of cancer cells injected into mice compared CCN2 also died earlier.
The researchers suspect that CCN2 is in ensuring the survival of tumor cells in hypoxic conditions played a role. If so, perhaps explain the CCN2 expression in tumor growth of cancer cells in the process of performance. They found that in cultured pancreatic cancer cells blocked CCN2 expression, will result in the death of cancer cells to hypoxia become much more sensitive. In addition, CCN2 in human pancreatic tumor samples expressed higher than other surrounding tissue, CCN2 expression in hypoxic cells appear to other associated protein expression. Finally, hypoxia itself will lead to pancreatic cancer cells CCN2.
Protein recent rejection of pancreatic cancer, and many other cells can also activate CCN2 expression conditions, including the presence of CCN2 itself. Cancer-related activation of other channels also increase its expression. As a result, a growing number of tumors that occur in the same event as the storm produced greater amounts of CCN2, thus leading to rapid tumor growth and metastasis.