In many findings or research articles researchers says that their molecules changed the expression of BCl2, Bax, PARP, p53,p21 etc. but in true sense how a molecules (even tiny) can cahnge the expression of a gene/protein without interacting with its process. Since many of these molecules do not directly or indirectly have interaction capability. May be these ratios only shows fraction in dead and live cells.
Hi,
I am not exactly sure if you want to start a discussion about clinical diagnostics or methods in general. During my PhD I treated renal tumor cells (cell culture) with tyrosin kinase inhibitors to analyze the down stream effects of the receptor inhibition (VEGFR, EGFR, PDGFR). I analyzed differences in the proteom (with Refraction-2D/2D-DIG) and with quantitative Western blots. I could see altereations in apoptosis regulation and the unfoldes protein responce. Bcl-2, Bcl-xL and other members of the Bcl-2 family have been found up or down regulated during the treatment (in comarison with untreated cells). With very heterogenous cancer cells the reproducibilty of Western blots is a big problem though.
So I think molecules in the meaning of drugs, inhibitors, enhancers, etc. do have an impact. The experimental design, choice of controles and choice of the used methods should be very well deliberated. Genomic as well as proteomic approaches should be used.
What do you think? Have you made different experiences?
Kind regards,
Kristin
I understood that you are asking the action mechanisms of molecules or compounds. If so, e.g., for Bcl-2 family inhibitors, the following paper will be useful.
https://www.ncbi.nlm.nih.gov/pubmed/28209992
Dr Hamada, my question is not about inhibitors of Bcl2 or Bax but is more general. I mean every/most anticancer compounds enhance Bax..how?
- Badges
- Science topic
- Similar topics
- Medicine
- Oncology
- Cancer Research