Presentation Title

Mitotic Gene Bookmarking by RUNX1 Stabilizes the Normal Mammary Epithelial Phenotype

Abstract

The epithelial to mesenchymal transition (EMT), a transdifferentiating process through which normal epithelial cells gain a more migratory and potentially invasive mesenchymal phenotype, is critical in both normal cellular development and the initiation of epithelial based cancers [1]. However, the epigenetic mechanisms that regulate the initiation of this process are not well understood. Studies by our group and others have shown occupancy of specific target genes by transcription factors such as RUNX1 throughout mitosis – mitotic gene bookmarking – is an important epigenetic mechanism to maintain cellular identity [2]. Accordingly, we have shown that disruption of RUNX1 function leads to alterations in epithelial cell proliferation, differentiation, and morphology [3]. The current study investigates the hypothesis that mitotic gene bookmarking by RUNX1 plays a critical role in the maintenance of the normal mammary epithelial phenotype and its disruption leads to the initiation of the EMT and potentially the onset of breast cancer.

References:

1. Tomaskovic-Crook, E., E.W. Thompson, and J.P. Thiery, Epithelial to mesenchymal transition and breast cancer. Breast cancer research, 2009. 11(6): p. 213.

2. Zaidi, S.K., et al., Mitotic Gene Bookmarking: An Epigenetic Program to Maintain Normal and Cancer Phenotypes. Mol Cancer Res, 2018. 16(11): p. 1617-1624.

3. Hong, D., et al., Runx1 stabilizes the mammary epithelial cell phenotype and prevents epithelial to mesenchymal transition. Oncotarget, 2017. 8(11): p. 17610.

Primary Faculty Mentor Name

Sayyed K. Zaidi

Secondary Mentor NetID

jstein7

Secondary Mentor Name

Janet Stein

Status

Graduate

Student College

Graduate College

Program/Major

Pharmacology

Primary Research Category

Biological Sciences

This document is currently not available here.

Share

COinS
 

Mitotic Gene Bookmarking by RUNX1 Stabilizes the Normal Mammary Epithelial Phenotype

The epithelial to mesenchymal transition (EMT), a transdifferentiating process through which normal epithelial cells gain a more migratory and potentially invasive mesenchymal phenotype, is critical in both normal cellular development and the initiation of epithelial based cancers [1]. However, the epigenetic mechanisms that regulate the initiation of this process are not well understood. Studies by our group and others have shown occupancy of specific target genes by transcription factors such as RUNX1 throughout mitosis – mitotic gene bookmarking – is an important epigenetic mechanism to maintain cellular identity [2]. Accordingly, we have shown that disruption of RUNX1 function leads to alterations in epithelial cell proliferation, differentiation, and morphology [3]. The current study investigates the hypothesis that mitotic gene bookmarking by RUNX1 plays a critical role in the maintenance of the normal mammary epithelial phenotype and its disruption leads to the initiation of the EMT and potentially the onset of breast cancer.

References:

1. Tomaskovic-Crook, E., E.W. Thompson, and J.P. Thiery, Epithelial to mesenchymal transition and breast cancer. Breast cancer research, 2009. 11(6): p. 213.

2. Zaidi, S.K., et al., Mitotic Gene Bookmarking: An Epigenetic Program to Maintain Normal and Cancer Phenotypes. Mol Cancer Res, 2018. 16(11): p. 1617-1624.

3. Hong, D., et al., Runx1 stabilizes the mammary epithelial cell phenotype and prevents epithelial to mesenchymal transition. Oncotarget, 2017. 8(11): p. 17610.