When a cell becomes cancerous, one of the thing to ensure survival is to multiply and move away from the original site to find food and ensure to escape immune surveillance. Indeed a localized cell will end-up being reported as it changes its receptors and membrane proteins. Its neighbors will tell on it as it will escape the consensus required and set in place by the NOTCH. But a normal cell is well specialized in order to participate to the Notch controlled function of the tissue to which it belongs. A cell in the liver, will be differentiated to do liver function. and the more a cell differentiate, the less it can multiply. For the cell that is now cancerous, one of the way to recuperate its multiplication potential is to de-differentiate, lose the differentiation, becoming more totipotential. It is known that forcing leukemic cell for example into full differentiation, will control the disease.
The finding that an epigenetic phenomena can return totipotentiality to the cell marks a significant discovery
XU et al :" that expression of microRNA-145 (miR-145) is low in self-renewing human
embryonic stem cells (hESCs) but highly upregulated during
differentiation. We identify the pluripotency factors OCT4, SOX2, and
KLF4 as direct targets of miR-145 and show that endogenous miR-145
represses the 3' untranslated regions of OCT4, SOX2, and KLF4." "Yamanaka factors (Oct3/4, Sox2, Klf4, c-Myc) are highly expressed in embryonic stem (ES) cells,"LIU ET AL
This means cancer cell have to suppress mi-145 to recoup self renewal...this is a powerful pathways that need to be absolutely tampered with particularly in hematologic malignancies!
GET BACK TO WORK WITH THE CRBCM! PROOF OF CONCEPT NEEDED!
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