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Frame et al. Investigating models for prostate cancer research
cause DNA damage, this was measured in two ways, the conclusions. This is why we advocate the use of a
comet assays [Figure 3B] and γH2AX foci [Figure 3C]. panel of cell lines, with an understanding of the origin
Both methods of measurement showed that stem-like of those cell lines, such that the relevance of the result
cells sustained less DNA damage following etoposide can be best understood. Cell lines are excellent tools to
treatment. Finally, Ki67 staining was carried out, and establish methods and make an initial determination of
this indicated that TA cells were more proliferative mechanism of action and effectiveness of a compound.
(50%-90% Ki67-positive cells) than stem-like cells However, our hypothesis is that use of patient-derived
(10%-60% Ki67-positive cells), with patient variability primary prostate epithelial cell cultures is more clinically
being observed [Figure 3D].
relevant and is more representative of intra-and inter-
Use of QPI to compare growth and proliferation of cell tumor heterogeneity [13,15,22,23] . Cell lines are usually
lines to primary prostate epithelial cells cultured from characterized by expression of certain markers, for
patient tissue. example whether they are androgen receptor positive
or negative [24,25] . However, an alternative strategy to
What these results and previous studies have shown compare the different cell types might be to look at cell
us is that the model that is used can strongly impact behavior. In order to do this we used a ptychographic
Figure 3: Prostate cancer stem-like cells (SC) sustain less DNA damage and form more colonies than progenitor cells following etoposide
treatment, which correlates with less proliferation. Cancer SC and transit amplifying (TA) cells were selected from primary prostate epithelial
cell cultures, treated with 30 µmol/L of etoposide and assessed for (A) colony forming ability, (B) comet assay, (C) γH2AX foci formation
and (D) Ki67 expression. Each symbol represents a patient sample
Journal of Cancer Metastasis and Treatment ¦ Volume 3 ¦ December 6, 2017 307