I'm doing a Knockdown experiment for a specific gene which has been associated with chromosome segregation. So I'm just wondering whether it will affect the efficacy of an anticancer drug if the KO cancer cells have mitotic defect.
Thanks
It is impossible to answer this question without doing the necessary laboratory work.
Depends on the whether the drug is cytostatic or cytotoxic and then how/what does the drug target?
Since the cells won't divide because of your induced mitotic defect you would not see any difference in IC50 with a cytostatic drug
A cytotoxic drug that kills cells during cell division think microtubule agents would have its IC50 increased because the cells won't enter mitosis (taxanes have biphasic killing so you would see the second toxicity at very high doses)
However something like TRAIL that induces apoptosis directly won't be affected by your Knockdown and will still kill the cells.
Think of the pathway the drug is hitting and that will tell you if you will see a shift in the IC50.
I guess first you have to answer multiple questions for a concrete conclusive answer for you question:
1. Is the gene over expressed in cancer? If yes, which cancers?
2. In which pathway, the gene product functions and what are the bypasses?
3. What is the phenotype of wilgtyoe KO/KD cells?
4. Possibility of inhibitor development, etc.
Could be it is a type of separase, but I hope for the best,
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