The mechanism of cancer tumor cells becoming cancer stem cells that can sustain long-term growth

International research, led by scientists from the London Creek Institute and the Hebrew University of Jerusalem, sheds light on the survival mechanisms in cancer cells that can re-emerge even after aggressive treatment. In a paper published in Science which also publishes some other studies on recombinant human proteins, the researchers describe the mechanism by which cancerous tumor cells become cancer stem cells that can sustain long-term growth.

When cancer develops, the resulting cells are heterogeneous in their biological properties and have different contributions to tumor development. Only a small percentage of cancer cells can form new tumors or metastases, and these are called "cancer stem cells". This difference between tumor cells constitutes a major challenge in understanding the nature of the tumor, its sensitivity to drugs and the effective treatment of all tumor cells.

"Many chemotherapeutic agents leave a small amount of cancer stem cells, causing disease to re-emerge after a few years," said Eran Meshorer, director of the Stem Cell and Epigenetics Laboratory of the Life Sciences Institute. "Therefore, it is important to identify cancer stem cells and characterize the differences between different tumor cells as a basis for detection of weaknesses during disease progression."

Cancer stem cells are not limited to the tumor itself. They can re-engage in a healthy environment and stimulate the disease. In order to study the characteristics of these unique cells, Prof. Dr. Meshorer and Dr. Alva Biran from the Hebrew University collaborated with Dr. Paula Scaffidi and Dr. Christina Morales Torres from the Crick Institute in London. The international team also includes Dr. Ayelet Hashahar Cohen of the Hebrew University, Dr. Rotem Ben-Hamo and Sol Efroni of Bar-Ilan University and Dr Tom Misteli of the NIH National Cancer Institute.



The team found that in many cancer types, those cancer stem cells lost one of their DNA packaging proteins, H1.0. By binding to DNA, the H1.0 gene was expressed.

"In order to understand the mechanism of action, we mapped the interaction pattern with DNA and found that it binds to the regulatory region of the gene," explained Professor Meshorer. "When the levels of H1.0 increase, these genes can inhibit the proliferation of cancer cells."

The study is based on epigenetics - a scientific field that investigates gene expression by switching the DNA on and off genes. To identify cancer stem cells from other cells in the tumor, the team studied the epigenetic mechanisms that differentiate at least sorted cells with infinite splitting properties and the potential to produce growth, as well as more sorted cells lacking this ability.

The results show an inverse relationship between H1.0 and cancer cell division: with the decrease of H1.0 levels, the greater the potential for uncontrolled division of the cells is. In contrast, high levels of protein prevent this process. We found that the disappearance of H1.0 protein is the characteristic of cancer stem cells, and it is necessary to maintain the ability to divide and the potential for growth.



This finding opens the door to medical intervention for cancer stem cells, aimed at restoring high levels of H1.0 in all cancer cells and blocking the differentiation of cancer cells. Although further research is needed to understand the usefulness of H1.0 protein in preventing cancer growth and spread, this study significantly expresses the cancer stem cell mechanism and relatively new epigenetic approaches to cancer research. Flarebio offers recombinant proteins of good quality such as recombinant Cd44 at good prices.