BioTek July 2019 - 20

tested. However, proliferation of the two cancer cell
types, HeLa and HCT116, was inhibited by 10 μM
cercosporamide. Treatment with doxorubicin resulted in the dose-dependent inhibition of NIH3T3,
HeLa and HCT116 cell proliferation. Quantitative
analysis of the effect of doxorubicin treatment over
time was provided by determining IC50 values using the area under the curve (AUC) from each proliferation profile (Figure 7). HCT116 had the highest
sensitivity to doxorubicin, followed by HeLa and
NIH3T3, with 4 nM, 5.1 nM, and 20.5 nM IC50 values, respectively.

Kinetic Phenotypic Analysis of Cellular
Response to Antiproliferation Drugs
To further examine the effects of doxorubicin treatment, experiment videos (video 1, video 2) were used
to conduct a qualitative evaluation of each cell type
at inhibitory concentrations of the drug. A significant decrease in NIH3T3 cell numbers was observed
within 36 hours at 10 nM doxorubicin, however no
obvious signs of apoptosis were present. These findings indicate that at this concentration doxorubicin
inhibits cell division without causing overt cytotoxicity. In contrast, NIH3T3 cells treated with 1 μM
doxorubicin exhibited considerable cytotoxicity and
signs of apoptosis within 24 hours (Figure 8).

Figure 6. NIH3T3, HeLa and HCT116 cell proliferation profiles enable
quantitative analysis of drug response. Cell counts per mm2 were calculated
every 2 hours for 5 days or until cells reached full confluence. Profiles from
5 drug concentrations demonstrate a cell type-dependent differential dose
response.

Figure 5. 96-well microplate matrix of HeLa cell proliferation over 5 days.

Figure 7. Measuring dose-dependent inhibition of cell proliferation by

Eight concentrations of doxorubicin and cercosporamide (4 replicates each)

doxorubicin. AUC of cell count per mm2 proliferation profiles were used to

were tested alongside negative controls.

calculate IC50 values.

BioTek July 2019

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