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Masatoshi Takeichi's discovery: What is the story behind E-cadherin?
In the world of cell biology, a protein called E-cadherin has become a key research focus. This protein has been implicated in the development of several cancers, such as stomach, breast, and colorectal cancer. However, the discovery of E-cadherin was not accidental, but the result of years of hard work and exploration by Japanese scientist Masatoshi Takeichi.
Takeichi began exploring cell-cell adhesion in 1966, and these studies ultimately led to the discovery of E-cadherin.
Takeichi's research originated from his studies on lens differentiation in chick embryos at Nagoya University. Through the accumulation of culture medium, he observed that the attachment rate of cells suspended in culture medium was delayed, which sparked his interest in cell adhesion. As his research progressed, he began to focus on the role of proteins, magnesium, and ions such as calcium, and eventually discovered the importance of calcium in cell-to-cell adhesion.
E-cadherin belongs to a class of membrane proteins called cadherins, which are calcium-dependent and play an important role in cell-cell adhesion. The structure of E-cadherin consists of five extracellular cadherin repeat units, a transmembrane region, and a highly conserved intracellular tail. These properties make it crucial for cell-cell interactions.
The function of E-cadherin is not limited to cell adhesion, but also involves cell proliferation inhibition and cell cycle regulation.
E-cadherin affects cell behavior during the cell cycle by contact inhibition of proliferation, which is achieved by inducing activation of the Hippo pathway. When the adhesion strength between cells decreases, such as when cell density decreases, cell proliferation will be promoted, making E-cadherin particularly important in regulating cell proliferation and migration.
In addition, the study showed that E-cadherin plays an important role in the formation of epithelial buds, a process that involves cell sorting and internal mechanical interactions. Different levels of epithelial tissue respond to growth factors and extracellular matrix in different ways, highlighting the diversity of E-cadherin in tissue development.
The inactivation of E-cadherin is closely related to the progression of various cancers. Reducing the expression of E-cadherin will increase the migration ability of cells and promote the spread of tumors.
The functional loss of E-cadherin can lead to the weakening of cell-to-cell connections, which has a direct impact on the invasiveness and metastatic ability of cancer cells. In many tumors, such as breast cancer and gastric cancer, the expression of E-cadherin is significantly reduced, which becomes one of the indicators for judging the malignancy of the tumor.
As the research on E-cadherin deepens, scientists gradually realize its importance in embryonic development. In the early stages of embryonic development, E-cadherin promotes the uniform differentiation of cells and the establishment of tissue structure, allowing cells to be sorted and assembled correctly.
Takeichi's research not only provides a basis for our understanding of the function of E-cadherin, but also opens up new perspectives on tumor biology and the nature of embryonic development. The presence of E-cadherin shows how cells interact with mechanical forces through chemical signals to regulate their shape and movement. As our understanding of this protein improves, new therapeutic strategies may be developed to combat tumors characterized by E-cadherin inactivation.
In summary, E-cadherin not only plays a core role in cell adhesion, but also reflects how cells maintain coordination in development and disease. From this perspective, can we explore new therapeutic methods to address the challenges of cancer by regulating the function of E-cadherin?
