Author: Zhang Siwei Date: 2018-08-23
Usually most breast tumors begin in the inner cells of the breast duct, which are surrounded by myoepithelial cells. Previously, scientists believe that the cell layer of myoepithelial cells is a static barrier to prevent cancer infiltration.
More recently, experiments conducted in laboratory-cultured mouse tissue by Johns Hopkins University in the United States have shown that the cell layer around the breast's milk duct can reach out and capture escaped cancer cells to prevent their spread in the body. This suggests that the cell layer of myoepithelial cells is an active defense mechanism that inhibits breast cancer metastasis. The results of the experiment were published online in the Journal of Cell Biology on July 30.
It is known that the myoepithelial layer is clinically used to diagnose differential breast cancer and invasive breast cancer in humans. If breast cancer cells break through the myoepithelial layer, the result is a so-called invasive cancer, which has a higher recurrence rate and requires more aggressive treatment.
"If cancer metastasis is seen as a long-distance race, breaking through the cell layer is equivalent to rushing out of the starting line." Professor of Cell Biology at Johns Hopkins University School of Medicine and John Hopkins Sidney King Andrew Ewald, a member of the Mel Comprehensive Cancer Center, said: "Understanding how cancer cells are restricted can help us develop ways to predict the risk of individual cancer metastasis."
In the study, Ewald and his team engineered cells removed from the inner mammary gland to produce the protein Twist1, which acts by altering gene expression and is involved in cancer metastasis of multiple tumor types.
Surprisingly, the researchers found that when infiltrating Twist1 cells broke through the myoepithelial layer, myoepithelial cells were able to capture these escaped cells. In a total of 114 observations, 92% of the time it was pulled back into the mammary duct.
Katarina Sirka, a Ph.D. student at Ewald Laboratories, said: "These findings establish a new concept for myoepithelial cells as a dynamic barrier against cell escape, rather than acting as a static barrier as previously speculated."
To confirm that their findings are an active behavior and not just due to the natural “stickiness†of cells, Ewald and his team changed two key features of myoepithelial cells: their ability to contract and their number of infiltrating cells. ratio.
First, the researchers genetically engineered mouse myoepithelial cells to remove their smooth muscle actin, a protein that causes cell contraction. In this case, the number of escape-infiltrating cells that broke through the myoepithelial layer was increased by a factor of three compared to normal myoepithelial cells as a control.
The researchers also found that reducing the ratio of myoepithelial cells to infiltrating cells also increased the number of escaped cancer cells. By adding two myoepithelial cells to each infiltrating cell, the escape rate is reduced to 1/4 compared to the diffusion of infiltrating cells without a defensive barrier.
Eliah Shamir, a surgical pathology researcher at the University of California, San Francisco, said: "This is important because it indicates that the physical integrity of myoepithelial cells and gene expression in myoepithelial cells are important for predicting the behavior of human breast tumors. Any muscle Where the cortex becomes thin or shed, there is a possibility that cancer cells will escape."
In the future, Ewald and his team plan to study the cellular mechanisms that drive the dynamic response of the myoepithelial layer and the causes of infiltration caused by its failure.
Source: Chinese Journal of Science
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