The plant extract, I have been working on, has a potent anti-tumor effect proven by several in vitro and in vivo studies. Through, the direct effect of the extract on tumor cells is not explained but it showed a synergistic effect with 5FU in renal cancer. Reduction of chemotherapeutic agent resistance-related genes and reduction of ICAM-1 (Intercellular Adhesion Molecule 1) expression in parallel with the reduction of nuclear factor-κB (NF-κB) expression were described as a possible mechanism.
Recently I have identified some steroids, phenolic compounds, and alkaloids in the plant extract. Based on the data mentioned above, can anyone suggest some potential target proteins for molecular docking studies of these isolated compounds (for anti-cancer activity)? What about VEGFR-2 and TNF-alpha or TNFR-1?
Well Cisplatin is one of a kind..
Once the Compound diffuses into the cell, it looses the chloride ions and directly cross- links between the DNA strand, mostly to the guanine group. This causes intra and interstrand cross linking resulting into inhibition of DNA. It also targets mitochondria to decrease ATPase activity causing cyto-toxicity.
Mr. Pradyumna Shejwalkar thanks for your suggestion. Actually, I am trying to solve the hypothesis mentioned in the previous study. So I am focusing only on the mechanisms that inhibit NF-kB signaling and searching for specific proteins that contribute to activating NF-kb signaling.
Well
NF-κB dimers are activated by IKK-mediated phosphorylation of IκB, which triggers proteasomal IκB degradation. This enables the active NF-κB transcription factor subunits to translocate to the nucleus and induce target gene expression.
Also regulatory non-enzymatic scaffold protein NEMO is also responsible for this !
I don't know much about about nemo but you can go to abcam website and there you can find about it !
I read it when I was learning about p50 & p65!
Bit sirely you can get more info there
Mr. Pradyumna Shejwalkar As I am new in research, there is a lot of confusion around. Thanks again for your detailed explanation.
This IκB degradation is a result of TNFr activation. That's why I selected TNF-alpha. If it goes wrong then I will go for Nemo or other related factors. You can check the attached image from Arshad Rahman et al. 2011.
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