CRISPRa-Mediated Activation Reveals Proliferation Dynamics in Estrogen Receptor Positive Breast Cancer Cells
Presentation Type
Poster
Presentation Type
Submission
Keywords
Biology, Cell Biology, Genetics, Epigenetics, Genomics, Biotechnology, CRISPR, Gene-editing, Gene-activation, Breast Cancer
Department
Biology
Major
Biology, B.A.
Abstract
The development of new cancer therapies is greatly hindered by the scarcity of actionable genetic targets. Most cancer therapies on the market are designed around inhibiting oncogenes or exploiting cancer dependencies, but while these targets have played an essential role in cancer treatment, their effectiveness is reduced by mutational heterogeneity.
To overcome this limitation in therapeutic development, more attention has turned to the role of epigenetics in cancer cell replication. For instance, it is increasingly recognized that some tumor cells have evolved mechanisms to silence genes detrimental to cell growth rather than inactivating them via mutational changes. Our hypothesis is that cancer cells may epigenetically silence genes with anticancer properties. Thus, our study aims to determine if reactivating epigenetically silenced genes alters the rate of cancer cell proliferation. Specifically, we have used a dCas9-CRISPRa system to selectively activate 7 genes with proposed involvement in proliferation of MCF7 breast cancer cells. Our results indicate that epigenetically activated genes can alter cell replication rates early after gene activation or induce changes in cell cycle exit at later stages of activation. These results provide strong proof of concept that epigenetically silenced genes can expand the repertoire of actionable targets in cancer treatment.
Faculty Mentor
Dr. J. Antonio Gomez
Funding Source or Research Program
Academic Year Undergraduate Research Initiative, Summer Undergraduate Research in Biology
Location
Waves Cafeteria
Start Date
10-4-2026 1:00 PM
End Date
10-4-2026 2:00 PM
CRISPRa-Mediated Activation Reveals Proliferation Dynamics in Estrogen Receptor Positive Breast Cancer Cells
Waves Cafeteria
The development of new cancer therapies is greatly hindered by the scarcity of actionable genetic targets. Most cancer therapies on the market are designed around inhibiting oncogenes or exploiting cancer dependencies, but while these targets have played an essential role in cancer treatment, their effectiveness is reduced by mutational heterogeneity.
To overcome this limitation in therapeutic development, more attention has turned to the role of epigenetics in cancer cell replication. For instance, it is increasingly recognized that some tumor cells have evolved mechanisms to silence genes detrimental to cell growth rather than inactivating them via mutational changes. Our hypothesis is that cancer cells may epigenetically silence genes with anticancer properties. Thus, our study aims to determine if reactivating epigenetically silenced genes alters the rate of cancer cell proliferation. Specifically, we have used a dCas9-CRISPRa system to selectively activate 7 genes with proposed involvement in proliferation of MCF7 breast cancer cells. Our results indicate that epigenetically activated genes can alter cell replication rates early after gene activation or induce changes in cell cycle exit at later stages of activation. These results provide strong proof of concept that epigenetically silenced genes can expand the repertoire of actionable targets in cancer treatment.