Article: Lannin, T; Su, WW; Gruber, C; Cardle, I; Huang, C; Thege, F; Kirby, B; “Automated Electrorotation Shows Electrokinetic Separation of Pancreatic Cancer Cells is Robust to Acquired Chemotherapy Resistance, Serum Starvation, and EMT”, Biomicrofluidics, 10 (6)
Abstract: We used automated electrorotation to measure the cytoplasmic permittivity, cytoplasmic conductivity, and specific membrane capacitance of pancreatic cancer cells under environmental perturbation to evaluate the effects of serum starvation, epithelial-to-mesenchymal transition, and evolution of chemotherapy resistance which may be associated with the development and dissemination of cancer. First, we compared gemcitabine-resistant BxPC3 subclones with gemcitabine-naive parental cells. Second, we serum-starved BxPC3 and PANC-1 cells and compared them to untreated counterparts. Third, we induced the epithelial-to-mesenchymal transition in PANC-1 cells and compared them to untreated PANC-1 cells. We also measured the electrorotation spectra of white blood cells isolated from a healthy donor. The properties from fit electrorotation spectra were used to compute dielectrophoresis (DEP) spectra and crossover frequencies. For all three experiments, the median crossover frequency for both treated and untreated pancreatic cancer cells remained significantly lower than the median crossover frequency for white blood cells. The robustness of the crossover frequency to these treatments indicates that DEP is a promising technique for enhancing capture of circulating cancer cells. Published by AIP Publishing.
Funding Acknowledgement: National Science Foundation [DGE-1144153, ECCS-1542081]; Cornell University’s Engineering Learning Initiatives; HHMI med-into-grad scholarship; Lester and Sheila Robbins Scandinavian Graduate Student Fellowship; Cornell Center on the Microenvironment and Metastasis from the National Cancer Institute Physical Sciences Oncology Center (NCI PS-OC) [U54CA143876]
Funding Text: This material is based upon the work supported by the National Science Foundation Graduate Research Fellowship Program under Grant No. DGE-1144153 (TBL). The authors would like to thank Cornell University’s Engineering Learning Initiatives (WWS), HHMI med-into-grad scholarship (FIT), and the Lester and Sheila Robbins Scandinavian Graduate Student Fellowship (FIT), for financial support. This work was partially supported by the Cornell Center on the Microenvironment and Metastasis through Award No. U54CA143876 from the National Cancer Institute Physical Sciences Oncology Center (NCI PS-OC). This work was performed in part at the Cornell NanoScale Facility, a member of the National Nanotechnology Coordinated Infrastructure (NNCI), which is supported by the National Science Foundation (Grant No. ECCS-1542081). Any opinions, findings, and conclusions or recommendations expressed in this material are those of the author(s) and do not necessarily reflect the views of the National Science Foundation.