Dielectrophoretic properties distinguish responses to estrogen and fulvestrant in breast cancer cells

Kruthika Kikkeri, Sepeedah Soltanian-Zadeh, Ayesha N. Shajahan-Haq, Lu Jin, Jeannine Strobl, Robert Clarke, Masoud Agah

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


The majority of breast tumors express estrogen receptors (ER), and are treated with endocrine therapy (ET) drugs to target ERs and estrogen (E2) biosynthesis in the management of early and metastatic ER + breast cancer. However, ∼50% of patients receiving an ET exhibit either intrinsic (de novo) resistance or acquire resistance to these treatments despite persistent expression of ER in the tumors. Thus, an assay to better predict the drug responsiveness of ER targeting ET drugs, such as fulvestrant (Ful) would be beneficial for clinical treatments. Here, we compared two genetically related cell lines isolated from ER+ MCF-7 human breast cells: the LCC1 (Ful-sensitive (s)) and LCC9 Ful-resistant (r)). Using passivated-electrode insulator-based dielectrophoresis (π DEP), the DEP profile of LCC1 and LCC9 Ful-response were compared. Ful-s LCC1 cells responded with a gradual crossover frequency (f0) shift from 700 kHz to 300 kHz over 72 h. The Ful-r LCC9 cells showed a gradual f0 shift from 100 kHz to 700 kHz over this time period. In response to E2, LCC1 cells showed a small f0 shift from 700 kHz to 600 kHz while LCC9 showed a large f0 change from 100 kHz to 800 kHz. There are no significant differences in gene pathway-specific mRNA expression between the LCC1 and LCC9 cells. Nevertheless, several mRNAs identified in an unbiased screen are differentially expressed in LCC1 and LCC9 cells including PALLD, ADAP1, SLC12A2, and TM4SF1. Investigation of these genes could begin to clarify how responses to ET translate into changes in cellular bioelectric properties and contribute to validation of DEP ET response biomarkers.

Original languageEnglish (US)
Pages (from-to)186-194
Number of pages9
JournalSensors and Actuators, B: Chemical
StatePublished - Dec 20 2018
Externally publishedYes

Bibliographical note

Funding Information:
This work was supported primarily by the National Science Foundation under award number ECCS-1310090. This material is also based upon work supported by the NSF Graduate Research Fellowship under Grant No. 478969 . Technical services for gene expression array were provided by the Genomics and Epigenomics Shared Resources at Georgetown University Medical Center that is funded through Public Health Service award 1P30-CA-51008 (Lombardi Comprehensive Cancer Center Support Grant).

Funding Information:
Dr. Ayesha Shajahan-Haq an assistant professor of oncology at Lombardi Comprehensive Cancer Center and co-director of the M.S. program in Tumor Biology at Georgetown University (Washington, DC) . Her research focuses on understanding the molecular mechanisms in cancer cells that acquire resistance to anti-cancer therapies using a systems biology approach, particularly in breast cancer. Currently, she is funded by a R01 grant from the NCI in a collaborative project to build an experimentally validated dynamic mathematical model, which captures key cellular adaptations to drug therapies over time. She earned a B.S. and a M.S. in biological sciences from Wright State University (Dayton, OH) in 1997 and 1999, respectively, and a Ph.D. in pharmacology in 2004 from the University of Illinois at Chicago (Chicago, IL). She completed her postdoctoral training in mechanisms of drug resistance in breast cancer from Georgetown University in 2008.

Publisher Copyright:
© 2018 Elsevier B.V.


  • Breast cancer
  • Dielectrophoresis (DEP)
  • Drug sensitivity
  • Estrogen receptor positive (ER+)
  • Fulvestrant (Ful)


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