Is it expected that MCF12A cells should show some level of cytotoxicity to anticancer compounds or drugs? If so, what could be the biochemical or physiological reason therefore?
I haven't worked with MCF12A, but I can clearly say yes for MCF10A. They are (just as almost all proliferating cells) strongly affected by cytotoxic compounds such as doxorubicin, paclitaxel or the apoptosis-inducing kinase Inhibitor staurosporine. The reason should be the fact that they are highly proliferative, just as cancer cells are. In general, MCF10A tend to be much more sensitive to any toxic treatment you apply to them, likely due to the fact that they are not transformed and therefore lack the apoptosis-suppressive pathways that are active in most cancer cell lines.
MCF12A breast epithelial cell line is considered "normal" with respect to several growth characteristics. Further, this cell line harbors functional p53 and pRb. Consequently, cells of this cell line are thought to respond to anticancer drugs in a way that is seen by normal epithelial cells. Considering this, it is likely that the cell line exhibit cytotoxicity upon treatment with anticancer drugs presumably in the p53 and Rb-dependent manner.
I have not worked with MCF12A cells, but with MCF10A. And they tend to be more sensitive compared to cancer cell lines to most cytotoxic drugs I tested so far (doxorubicin, paclitaxel, the kinase Inhibitor staurosporine). The physiological reasons for that should be the fact that these cells proliferate a lot and that they lack the anti-apoptotic aberrations that most cancer cell lines have acquired.