The protein that turns normal cells into cancer stem cells offers a target to fight colon cancer
Due to the jaws, all vertebrate mammals can consume food using various techniques such as biting, chewing, and handling food. But did you know what chemical is behind the formation of this mouth frame?
We would not have developed our upper and lower jaw, as well as the tips of the teeth, the palatal shelves, including some parts of the brain and bones, if there had not been SATB2.
What is SATB2?
The AT-rich special sequence-binding protein 2 or called SATB2, is a DNA-binding protein. We can find it through an expression of epithelial cells of the colon and rectum, and also in the neurons of the brain. It plays an active role in chromatin remodeling and regulation of gene transcription. Its ability to bind AT-rich DNA sequences is known as the matrix-binding region or (MAR). And thanks to MAR, it can code for proteins in the body.
While a mutation in SATB2 is one of the main causes of a variety of diseases such as osteoporosis, neurodevelopmental disorders and speech impairment, it also exposes us to colorectal cancer.
Colon cancer, which is a global threat that puts the lives of patients around the world at risk. Being a metastasis, it is resistant to various anticancer drugs and therapies, including chemotherapy, radioactive treatments, and others. Therefore, patients may experience risks of relapse once their cells in the tumors resurface to bother them again and gradually bring them to the brink of death.
Researchers at LSU Health New Orleans School of Medicine and the Stanley S. Scott Cancer Center have highlighted this new discovery. They reported it in their online publication in Nature Research’s Scientific reports. According to their findings, SATB2 is a new protein, which lives near the colon and becomes malignant.
Since it has metastatic characteristics, it can grow faster and spread, and also mimic other stem cells in the body to become cancer stem cells.
Elaborate insight into the find
SATB2 is a protein with a built-in on / off signaling pathway capability. By flipping that switch, you signal a certain cancer cell to turn on or off. With the activation of certain signals, cancer cells can turn into cancer stem cells and appear to function according to the instructions of the signal.
Dr. Shrivastava compared healthy colorectal cells to colorectal cancer cells and found that healthy epithelial cells in colon tissues do not include activated SATB2 proteins, whereas it is highly activated in colorectal cancer cells.
To measure the performance of SATB2, the research team developed additional copies of the same proteins in normal cells. These cells were revealed to have evolved to differentiate and proliferate as a cancer stem cell with an improved growth rate.
And once SATB2 expressions are turned off, they do not mimic the characteristics of cancer stem cells, and colon cell growth is also suppressed. Along with this, it encourages the prevention of cancer cells from transforming into cancer stem cells.
Dr. Shrivastava believes that it is possible to achieve a new drug or therapy and a better diagnostic process based on the finding of a higher expression capacity of SATB2 in colorectal tissues or cells. In addition to this, it could be used as a novel marker to identify the severity of colon cancer in patients.
Now, we can be hopeful about the new finding of an agent that can prevent SATB2 from affecting stem cells in colon tissues to cause colorectal cancers and other forms of cancer as well.