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Using the cultured cell line as a tumor model, the researchers found that a tumorigenic virus-derived oncoprotein, v-Src, interacts with intracellular focal adhesion kinase (FAK) and stimulates a series of proteins within the cell. The interactions eventually block some cell surface proteins such as membrane-type matrix metalloproteinase 1 (MTl-MMP) into the cells by endocytosis. MT1-MMP is caused to accumulate on the surface of cancer cells, which further activates matrix metalloproteinase 2 (MMP2). The two proteins synergistically degrade matrix components that act as cell adhesion, resulting in loss of anchor junctions and metastasis of cancer cells.
According to Jun-Lin Guan, we discovered a tumor-specific pathway. The therapeutic drugs for this pathway can specifically interfere with the function of cancer cells without affecting the function of normal cells, which in turn can reduce the toxic effects of chemotherapy. reaction.
When cancer spreads, the patient usually dies - this is why many cancer research and drugs focus on the metabolic pathways that cause cancer cells to metastasize. Now, researchers at Cornell University have a better understanding of how these approaches work. Their research will likely promote the study of drugs that can interfere with the series of events leading to cancer metastasis. The results of the study are published in Developmental Cell Magazine (Volume 9, August 2005).
This study reveals how connective tissue that fixes cancer cells in one place can degenerate, "pull out" the diseased cells and spread it to other parts of the body. Researchers have identified a unique approach to cancer and believe that if drugs can be found that target this pathway, it could become a drug that does not affect normal cell function but affects cancer cell activity.
Guan and colleagues used a cultured mouse cell line to study cancer. The researchers used these cells to create a cancer cell model system, which means that its underlying pathway exists in the real-world system.
In this model system, the researchers discovered key differences in the mechanism of endocytosis between cancer cells and normal cells. They use a protein called v-Src produced by an oncogenic virus. This virus can stimulate normal cells to become cells with similar characteristics of cancer cells. Although this virus is not found in humans, it can lead to the growth of chicken tumors and produce cancerous cells in culture systems.
In the study, the researchers found that v-Src can attach to intracellular focal adhesion kinase. When another protein called MT1-MMP accumulates on the cell surface, it degrades the connective tissue that fixes the cancer cells. The accumulation of MT1-MMP also activates an enzyme called MMP2, which further degrades connective tissue. In this way, cancer cells take off their palates and spread to other parts of the body.
Although v-Src has not been found in human cancer patients, other cancers are indeed associated with this virus, including the herpes virus and cervical cancer associated with it.
Study Finds New Mechanism of Tumor Metastasis
Researchers at Cornell University in the United States discovered the mechanism of tumor metastasis and revealed how cancer cell junctions in the tumor foci are degraded, causing the cancer cells to break away from the original lesion and then undergo a series of processes of metastasis. The results of this study are useful for in-depth study of drug treatment targets that interfere with tumor metastasis. The results were published in the August issue of Developmental Cell Vol. 9, August 2005.