February 3, This article has been reviewed according to Science X's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility:. Anna de Sommer Champalimaud e Dr. Carlos Montez Champalimaud. Their results have now been published in Cancer Discovery. This has now prompted these researchers to further analyze what is at the root of this difference in cancer initiation potential. Are there specific mechanisms in the stem cells that make them competent?
To address this question, they performed, in animal models, a so-called transcriptional profiling of both oncogene-expressing skin stem cells and skin progenitor cells. Essentially, this consisted in comparing the genes expressed in stem and progenitor cells of the mouse skin that had their oncogenes cancer-causing genes activated.
They were thus able to identify several genes that were upregulated overexpressed in the activated stem cells, and this is what put them on the track to finding Survivin, also known as BIRC5.
Interestingly, the Survivin gene is highly expressed in most human cancers, such as lung, pancreatic and breast cancers, relative to normal tissues; it is an anti-apoptotic pro-survival gene that plays a key role during cell division. In order to determine whether Survivin really plays a role in basal cell carcinoma initiationβand formationβin stem cells, the team decided to delete the gene in their genetic mouse models following the activation of cancer-causing genes.
They hypothesized that, if Survivin was required for tumor formation, its deletion would render the stem cells unable to generate a tumor. And that's exactly what they saw. The next question the team asked was: would overexpression of the Survivin gene now make progenitor cells also able to initiate a tumor? This effectively made progenitor cells able to make basal cell carcinoma tumors.
