Breast cancer cell obatoclax response characterization using passivated‐electrode insulator‐based dielectrophoresis

• Published in: Electrophoresis Vol. 38; no. 16; pp. 1988 - 1995
• Main Authors: Soltanian‐Zadeh, Sepeedah, Kikkeri, Kruthika, Shajahan‐Haq, Ayesha N., Strobl, Jeannine, Clarke, Robert, Agah, Masoud
• Format: Journal Article
• Language: English
• Published: Germany Wiley Subscription Services, Inc 01.08.2017
• Subjects: Anticancer properties; Antineoplastic Agents - pharmacology; Biotechnology; Breast cancer; Breast Neoplasms; Cancer; Cell Proliferation - drug effects; Cell Size - drug effects; Dielectrophoresis; Dielectrophoresis (DEP); Drug Resistance, Neoplasm; Drug sensitivity; Electrical properties; Electrodes; Electrophoresis - instrumentation; Electrophoresis - methods; Estrogen Antagonists - pharmacology; Estrogen receptor positive (ER+); Estrogens; Female; GX15‐070 (Obatoclax); Humans; MCF-7 Cells; Microfluidic Analytical Techniques; Pyrroles - pharmacology; Sensitivity analysis; Trapping; Breast cancer; Dielectrophoresis (DEP); Estrogen receptor positive (ER+); GX15-070 (Obatoclax); Drug sensitivity
• ISSN: 0173-0835; 1522-2683
• DOI: 10.1002/elps.201600447

Inherent electrical properties of cells can be beneficial to characterize different cell lines and their response to experimental drugs. This paper presents a novel method to characterize the response of breast cancer cells to drug stimuli through use of off‐chip passivated‐electrode insulator‐based dielectrophoresis (OπDEP) and the application of AC electric fields. This work is the first to demonstrate the ability of OπDEP to differentiate between two closely related breast cancer cell lines, LCC1 and LCC9 while assessing their drug sensitivity to an experimental anti‐cancer agent, Obatoclax. Although both cell lines are derivatives of estrogen‐responsive MCF‐7 breast cancer cells, growth of LCC1 is estrogen independent and anti‐estrogen responsive, while LCC9 is both estrogen‐independent and anti‐estrogen resistant. Under the same operating conditions, LCC1 and LCC9 had different DEP profiles. LCC1 cells had a trapping onset (crossover) frequency of 700 kHz and trapping efficiencies between 30–40%, while LCC9 cells had a lower crossover frequency (100 kHz) and showed higher trapping efficiencies of 40–60%. When exposed to the Obatoclax, both cell lines exhibited dose‐dependent shifts in DEP crossover frequency and trapping efficiency. Here, DEP results supplemented with cell morphology and proliferation assays help us to understand the response of these breast cancer cells to Obatoclax.