黑色素细胞 z-bo 2020-09-19 413

　　Melanocytes accumulate in the skin, and melanin is secreted by melanocytes. Hokuro is a benign tumor. Previous studies have shown that mutations in the BRAF gene can cause melanocytes to expand. However, the mechanism by which the accumulation of these cells stops after mol formation has not been clearly studied.

　　Recently, researchers at the Perelman School of Medicine at the University of Pennsylvania discovered an important genetic factor p15, which has the ability to regulate plaque cells and maintain a benign non-growth state. BRAF mutations may allow the mother’s repair cells to grow and regulate the expression of tumor suppressor protein p15. If the inhibitory effect of p15 disappears and cell division continues, a normal skull becomes a melanoma. Researchers have established a special human melanoma model. While suppressing the expression of melanosome p15, it mutated other important factors in the formation of melanoma, and used histology to transplant transgenic skin tissue into experimental mice. It was found that when p15 protein is no longer expressed, melanocytes become cancer and develop into melanoma.

　　The focus of this research is the combination of medicine and melanite culture. It cultivates melanite in a three-dimensional life state, which can be used for functional research.

　　The reason why hokuro stops growing

　　Both hokuro and melanoma are derived from cells that secrete melanin in the skin. Scientists for only a few decades have studied the BRFA gene mutations that cause melanocytes to proliferate, and benign scallops and malignant melanomas are rare. In a normal pillow, when the number of melanocytes reaches a few millimeters, the cells stop expanding. why is it like this? The field of research has been confusing for a long time. To find out, the researchers studied normal melanocytes in the patient's skin and melanoma in the patient's skin, and used unblemished normal skin melanocytes as a blank control. This study found that the p15 content of melanocytes in moles is 140 times that of normal skin melanocytes. Cancerous melanosomes have little or no p15.

　　This means that p15 plays an important role in the regulation of benign or malignant skulls, and the sudden down-regulation of p15 can lead to melanocyte carcinogenesis. Overexpression of the BRAF gene will cause hokuro cells to secrete the signal molecule TGF-β, thereby feeding back the regulation of p15. The combination of these findings raises a hypothesis as to why hokuroku stopped growing. Most hokuroku secrete an appropriate amount of TGF-β to stop cell division after reaching a diameter of at least a few millimeters.

　　P15-the "risk" of skull cancer

　　Many researchers focused on another related tumor suppressor protein, p16, which inhibits the growth of skull cells. The gene encoding p16 is physically close to the gene encoding p15. In the cell

　　Decreased expression of p15 in

　　can cause canceration of melanocytes. Although these two tumor suppressors have the same functions, researchers have recently discovered that p15 also has specific functions. For example, expression of p15 in normal cells can completely stop cell division. p16 slows down the split speed. This shows that p15 also contains other functions, but they are ignored. Researchers will conduct in-depth research on the experiments and model establishment of melanoma expansion, and combine the findings with treatment.