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 frame of the mouth?

We would not have developed our upper and lower jaws, as well as the buds of the teeth, the palatal shelves, including some parts of the brain and the bones, if there had been no SATB2.

What is SATB2?

Special AT-rich Sequence-Binding Protein 2 or known as 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 to AT-rich DNA sequences is known as the matrix attachment region or (MAR). And because of 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 difficulties, it also exposes us to colorectal cancer.

A colon cancer, which is a global threat to put at stake the lives of patients around the world. Being a metastasis, it is resistant to various cancer drugs and therapies, including chemotherapy, radioactive treatments and others. Therefore, patients may experience risks of relapse once their cells in the tumors re-emerge to bother them again and gradually bring them to the brink of death.

This new discovery has been brought into the spotlight by researchers at LSU Health New Orleans School of Medicine and the Stanley S. Scott Cancer Center. They reported it in their online publication in Nature Research’s scientific reports. According to their findings, SATB2 is a new protein that lives near the colon and becomes malignant.

Since it has metastatic features, it can grow faster and spread, and also mimic other stem cells in the body to become cancer stem cells.

Opinion elaborated on the finding

SATB2 is a protein with a built-in on/off signaling pathway capability. Using that switch tells a certain cell in the cancer cells to turn on or off. With the activation of certain signals, cancer cells can become cancer stem cells and appear to function according to the signal’s instructions.

Dr. Shrivastava compared healthy colorectal cells with colorectal cancer cells and found that healthy epithelial cells in colon tissues do not contain activated SATB2 protein, whereas in colorectal cancer cells it is highly activated.

To measure the performance of SATB2, the research team grew additional copies of the same proteins in normal cells. These cells were revealed to have evolved to differentiate and proliferate as cancer stem cells with an enhanced growth rate.

And once SATB2 expressions are turned off, they don’t mimic the characteristics of cancer stem cells, and colon cell growth is also suppressed. Along with this, it promotes the prevention of cancer cells from transforming into cancer stem cells.

Dr. Shrivastava believes that it is possible to generate a new drug or therapy and a better diagnostic process based on the finding of increased 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.