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The secret connection between cells: Why is E-cadherin the silent killer of cancer?
In the field of cancer research, E-cadherin, a transmembrane protein, has attracted great attention from scientists. Its existence is essential for maintaining adhesion between cells, and its abnormalities may lead to the development of a range of cancers, including gastric cancer, breast cancer, colon cancer, and ovarian cancer.
E-cadherin is a calcium-dependent cell-cell adhesion glycoprotein mainly expressed in epithelial tissues. This protein is encoded by the CDH1 gene and plays an important role in connections between cells. When E-cadherin function is lost or expression is reduced, cell adhesion is weakened, making cells easier to move and more likely to invade surrounding tissues across the basement membrane, increasing the risk of cancer metastasis.
The basic function of E-cadherin is to promote cell communication and support tissue stability, but when this system is damaged, it can become a promoter of cancer.
Past research has shown that mutations in E-cadherin, a tumor suppressor gene, are associated with various cancer types. In particular, studies on breast and gastric cancer have found that the loss of E-cadherin is directly linked to the increased invasiveness of cancer cells. Especially in invasive ductal carcinoma of breast cancer, the expression of E-cadherin is significantly reduced, making cells more susceptible to epithelial-mesenchymal transition (EMT). This process is closely related to the migration and metastasis of cancer cells.
The history and discovery of E-cadherin
The discovery of E-cadherin can be traced back to 1966, when Japanese scientist Masatoshi Takeuchi first explored the adhesion mechanism of epithelial cells. His research initially focused on lens differentiation in chicken embryos. As his interest in cell adhesion deepened, he discovered a variety of cadherins and eventually determined the existence of E-cadherin. This discovery paved the way for later cancer research, revealing how cells use this adhesion protein to maintain tissue integrity.
The relationship between E-cadherin and cancer
Many studies have shown that impaired E-cadherin function is closely related to tumor progression and metastasis. In breast cancer, the downregulation of E-cadherin is often accompanied by the release of β-catenin, which can promote cancer cells to enter the mesenchymal state and thereby improve their migration ability. This process is undoubtedly critical to the growth and spread of cancer cells.
The loss of E-cadherin promotes the invasiveness of cancer cells, a phenomenon that has aroused great interest in it as a potential therapeutic target.
Functional mechanism of E-cadherin
E-cadherin not only participates in cell-to-cell adhesion, but also plays an important role in cell signaling. It regulates cell growth, migration, and shape by interacting with a variety of proteins. The internal structure of E-cadherin combined with the cytoskeleton helps maintain the shape of the cell and provides stable traction during cell migration.
During development, E-cadherin is critical for the formation of multicellular organisms. Its adhesion function in embryonic development not only supports the organizational structure of cells, but also promotes the correct differentiation of cells at the right time and place.
Clinical significance
Because of the direct correlation between the loss of E-cadherin and various cancers, the medical community began to use E-cadherin as a tumor biomarker. By testing the expression of E-cadherin in patients, doctors can assess the type of cancer and its potential aggressiveness. Especially in the treatment of breast cancer, the detection of E-cadherin has become an important indicator for diagnosis.
In the study of hereditary breast cancer, mutations in the CDH1 gene are thought to be associated with increased tumor risk. This reminds us that genetic mutations are not only the culprits of genetic diseases but can also be promoters of cancer development.
Future research directions
With in-depth research on the function of E-cadherin, scholars have gradually realized that exploring the role of this protein in the tumor microenvironment and its interaction with other signaling pathways will be a focus in the future. This may not only improve our understanding of tumor biology but may also aid in the development of new treatment strategies.
In this evolving field, the revelations brought by E-cadherin remind us how the subtle connections between cells are established in the early stages of life and affect the final tumor behavior?
