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The mysterious role of E-cadherin: How does it affect our cell adhesion and tumor development?
E-cadherin, also known as epithelial adhesion protein, is an important cell-cell adhesion protein that is essential for maintaining the structure and function of tissues. E-cadherin, encoded by the CDH1 gene, plays an important role in many cancers, including gastric, breast, colon, thyroid and ovarian cancer. This article will provide an in-depth look at the function of E-cadherin, its significance in cell adhesion, and its potential impact in tumor development.
E-cadherin is responsible for stabilizing epithelial tissue in adhesion between cells and is a regulator of intercellular material exchange.
Since 1966, the discovery of E-cadherin has been promoted by Japanese biologist Masatoshi Takeuchi. His initial research focused on lens formation in chicks, and by analyzing cell cultures in the eye, he realized that cell-cell adhesion was critical to maintaining the integrity of the cell structure. E-cadherin is designed to be calcium-dependent and has five super-external cadherin repeating units. These structures work together to assist cell adhesion.
In epithelial cells, E-cadherin maintains tissue integrity and forms connections around the cell, thereby supporting the internal structure and function of the cell. Its degradation or loss of function has been considered to be closely related to tumor development, leading to increased cell proliferation, invasion, and metastasis.
When the function of E-cadherin is lost, the strength of cell adhesion decreases, which may make it easier for cancer cells to cross the basement membrane and invade surrounding tissues.
The occurrence of tumors is often related to the "epithelial-to-mesenchymal transition" (EMT), and E-cadherin plays an important role in this transition. During EMT, the expression level of E-cadherin decreases, causing cells to lose their tight adhesion properties, which enables them to become aggressive tumor cells. As tumors progress, cells often undergo a transition from an epithelial to a mesenchymal state.
Cellular mechanism of E-cadherin
The interaction of E-cadherin's internal structure with the cytoskeleton is key to its function. When E-cadherin forms connections between cells, it forms a complex with α-catenin and β-catenin, which ensures cell-to-cell adhesion. This adhesion not only affects the structure of the tissue, but also transmits signals between those adherent cells, which initiate different biochemical pathways that affect cell growth and movement.
E-cadherin also plays a role in the cell cycle: its adhesion can inhibit cell proliferation because E-cadherin triggers a mechanism of cell contact inhibition, which helps regulate cell density. When cell density decreases, the function of E-cadherin is affected, prompting cells to re-enter the cycle for proliferation.
The loss of E-cadherin is also associated with a significant increase in the ability of cancer cells to metastasize, making it easier for cells to invade surrounding tissues.
The relationship between E-cadherin and cancer
In many cancer types, the loss of E-cadherin function is a key factor in tumor metastasis. Taking breast cancer as an example, invasive ductal carcinoma has significantly different expression of E-cadherin than invasive lobular carcinoma. The expression of E-cadherin in invasive lobular carcinoma is usually significantly reduced, which increases the invasiveness and promotes the spread of cancer cells among tissues.
In addition, CDH1 mutations in the maternal genetic state are further associated with certain types of cancer, such as hereditary diffuse gastric cancer. However, mutations in the CDH1 gene often lead to the inactivation of E-cadherin, forming an unfavorable microenvironment and promoting tumor occurrence.
Future research directions
There are still many unanswered questions about the function of E-cadherin and its role in cancer. Future research on the regulatory mechanism of E-cadherin, the dynamic process of cell adhesion, and its specific performance in different cancer types may bring new breakthroughs in cancer therapy, such as the development of therapies targeting the E-cadherin pathway to improve Effectiveness and precision of cancer treatment.
Faced with these challenges to E-cadherin, we can’t help but wonder: Can we find an effective way to restore the function of E-cadherin in the future to combat the metastasis and development of cancer?
