I got an interesting results today:
I treated 2 myeloma cells(MM1.S and RPMI8226) with our one compound in the medium with 1% and 10% FBS, respectively, for only 4 hours. Prior to compound treatment, no serum starvation was applied to cell culture( low FBS started with compound treatment at same time). Then, Caspase 3 cleavage was examined in Western blot after harvesting cells upon treatment with our compound for 4 hours.
Results:
Caspase 3 cleavage was observed only in MM1.S cells treated with our compound in 1% FBS medium, but not in 10% FBS medium. In RPMI8226 cell, No Caspase 3 cleavage by our compound was detected in both 1% FBS and 10% FBS medium.
Question:
1.
Because I did not do serum starvation on cells before compound treatment, and compound treatment duration is very short(4 hours), so, capase 3 cleavage in MM1.S cells should not be relevant to serum starvation. Accordingly, I think that there may be something in FBS(serum) inhibiting capase 3 cleavage. Could someone let me know the apoptosis inhibitors in FBS? Many thanks.
2.
I feel very bewildered for the difference of Caspase 3 cleavage in MM1.S and RPMI8226 cells treated with our compound. I knew both cells harbor k-Ras mutation. Do you know any other differences between MM1.S and RPMI8226 cells in the background of genetics and epigenetics? Many thanks.
I will check more cell lines for Caspase 3 cleavage with our compound.
Thank you again.
Basal ROS in cells could be the answer for both of your questions. Serum has ROS inhibiting ability. See my paper.
https://www.researchgate.net/publication/299607409_Novel_PKC-_to_p47phox_interaction_is_necessary_for_transformation_from_blebbishields
Article Novel PKC-? to p47phox interaction is necessary for transfor...
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