In our experiment, we are checking and comparing two synthetic chemical compounds' impact on the expression levels of apoptotic and proto-oncogenic genes including p53, Bcl-2, cMyc, hTERT, and MMP13. But, we got an interesting and unexpected result. Our qPCR results showed that the expression of the P53 gene increased compared to the control, and the expression of the other genes also shows an increased expression level compared to the control. While we expect the expression of proto-oncogenetic genes (Bcl-2, cMyc, hTERT, and MMP13) to decrease.
Do you think there is a scientific explanation for this discrepancy?
Attached you can find our results.
The apoptotic process is modulated by various tumor suppressor genes, including P53 and proto-oncogenes. After DNA damage, some cellular responses are triggered by transcriptional activation of P53 and BCL-2 family proteins in order to maintain the integrity of healthy cells. The activation of P53 leads to either DNA repair and recovery or to apoptosis. Moreover, the effect of P53 on apoptosis has been shown to occur through the regulation of BCL-2 family genes The expression of P53 and Bcl2 genes increases similarly during this process because cytoplasmic p53 interacts with proapoptotic Bcl-2-family proteins, causing the permeabilization of mitochondria and apoptosis.
Dear Dr. Gharbavi,
Thank you for your reply. But I mean the expression of the BCL-2 gene, not it's family. Would you please tell me the rationale behind the overexpression of other genes like c-Myc, and hTERT?
Thank you
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