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E-cadherin loss of function: how does it make cancer cells more aggressive?
In cancer research, the dysfunction of E-cadherin has attracted the attention of many scientists. As an important cell adhesion protein, E-cadherin plays an extremely important role in the indirect interactions of healthy cells. When the function of this protein is lost, the behavior of tumor cells changes dramatically, making them more aggressive and increasing their ability to metastasize. This article will take a closer look at the role of E-cadherin and its association with cancer cell invasiveness.
E-cadherin is the key to maintaining adhesion between epithelial cells. When its expression is reduced, the adhesion between cells is weakened and the motility of cells is improved.
Biological role of E-cadherin
E-cadherin is a calcium-dependent cell-cell adhesion protein present in many epithelial cells. Its structure consists of five external cadherin repeats, a transmembrane region, and a highly conserved intracellular tail. E-cadherin is not only involved in the connection between cells, but also plays a key role in intracellular signaling. When E-cadherin expression in cells is normal, it can inhibit cell proliferation and promote cell apoptosis, thereby protecting the stability of epithelial tissue.
Loss of E-cadherin function affects cell proliferation, invasiveness and metastasis, which are closely related to the progression of cancer.
The association between E-cadherin inactivation and cancer
When E-cadherin expression is reduced or inactivated, the behavior of tumor cells changes. Cancer cells are able to break away from the original tumor, enhance their migration ability, and ultimately form metastases. Scientists have shown that the inactivation of E-cadherin is directly linked to the progression of several cancers, such as gastric cancer, breast cancer, and colorectal cancer.
In breast cancer, decreased E-cadherin expression is often associated with increased invasiveness of cancer cells, particularly in invasive lobular carcinoma compared to invasive ductal carcinoma.
Epithelial-mesenchymal transition (EMT) and E-cadherin
The transformation process - epithelial-mesenchymal transition (EMT) is an important process by which cancer cells acquire invasiveness. E-cadherin plays a key role in this process. When E-cadherin expression is inhibited, β-catenin is released from the cell membrane into the cytoplasm, further inducing the expression of transcription factors that promote EMT, which promote the transition of cancer cells to mesenchymal cells and enhance their invasiveness.
Cancer cell motility and E-cadherin
E-cadherin is also involved in regulating cell motility, which is crucial for tumor cell metastasis. Specifically, E-cadherin coordinates cell movement by providing binding between cells. When its function is impaired, cells lose their sense of direction, resulting in random movement and an inability to effectively migrate to new locations.
Clinical significanceIn gene knockout experiments on cell migration, the loss of E-cadherin caused cells to lose their sense of direction in movement, highlighting its importance in cell migration.
The expression status of E-cadherin has become a marker for the prognosis of some malignant tumors. For example, in breast cancer, the loss of E-cadherin is an indicator of poor prognosis. In addition, E-cadherin is also used as a diagnostic tool in cancer pathology, which can effectively help determine the type and malignancy of the tumor.
In many cases, complete loss of E-cadherin indicates that the tumor may be more aggressive and have a worse treatment prognosis.
New treatment opportunities
Understanding the function of E-cadherin and how it affects cancer cell behavior brings new hope for future tumor treatment. Therapies that restore E-cadherin expression or enhance its function have the potential to become a powerful tool for reversing cancer progression. Researchers are actively looking for ways to alter the regulation of E-cadherin as a potential therapeutic strategy.
As the research on E-cadherin deepens, we can't help but ask, can we change the fate of cancer cells or even save lives by regulating E-cadherin?
