The team of scientists at the Free University of Brussels, Belgium, first identified the cellular origin of basal cell carcinoma, the most common form of skin cancer.
Our skin stays healthy with the stripping of dead cells and is replaced by new ones. This process is controlled by progenitor cells, which differentiate into functional skin cells that replenish dead skin. At the same time, healthy skin is supported by a small number of stem cells. These stem cells usually remain "silent," but when the skin is destroyed, they are activated to help repair the skin.
However, when an error occurs in the above process, it may cause cancer. DNA damage or activation of oncogenes triggers a cascade of reactions that ultimately lead to abnormal cell proliferation and cancer. Some of these tumors may be benign, but some tumors spread throughout the body and are often referred to as metastatic tumors. Scientists have long been interested in what type of cells are responsible for the formation of tumors and how these cells are involved in the process of tumorigenesis and growth.
In this new study, scientists used mouse models to reveal how skin stem and progenitor cells respond when oncogenes are activated. Studies have found that progenitor cells can cause benign lesions, while only stem cells have the ability to develop into fatal invasive tumors.
In the study, scientists used a transgenic mouse model to activate oncogenic genes in stem and progenitor cells by altering mouse genes. At the same time, the researchers added fluorescent markers to oncogenes. In this way, cells that are activated by oncogenes are easily identified. In addition, progeny cells can also be tracked when these cells proliferate. These associated fluorescent cells are called "clones"
Item number
product name
CAS
characteristic
package
Price¥
C16-P10687
O-phthalaldehyde (OPA)
643-79-8
99% for
HPLC fluorescent labeling
1g
169
5g
378
Using mathematical models to analyze the number of fluorescently labeled cells in each clone, it was found that only "clones" derived from mutant stem cells can overcome the mechanism of programmed cell death, continue to divide and proliferate, and eventually develop into basal cell carcinoma (1 Skin cancer). Conversely, as the level of apoptosis increases, the growth of progenitor-derived "clones" will be "blocked", eventually leading to benign lesions. Targeting pathways that regulate cell fate is expected to be an effective way to prevent tumorigenesis or growth, or to create new treatment options.
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