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conferenceseries
.com
6
th
World Congress on
October 16-18, 2017 | San Francisco, USA
Breast Cancer & Therapy
Volume 2, Issue 5 (Suppl)
Breast Can Curr Res, an open access journal
Breast Cancer Congress 2017
October 16-18, 2017
Ets1
and
ESE1
reciprocally regulate expression of ZEB1/ZEB2, dependently on ERK1/2 activity, in breast
cancer cells
Nguyen Duy Sinh
1
, Kaori Endo
1
, Keiji Miyazawa
1
and
Masao Saitoh
1, 2
1
University of Yamanashi, Japan
2
University of Medicine and Pharmacy, Vietnam
T
he epithelial–mesenchymal transition (EMT) is a crucial morphological event that occurs during progression of epithelial
tumors. We reported previously that levels of the δEF1family proteins (ZEB1/δEF1 and ZEB2/SIP1), key regulators of the EMT,
are positively correlated with EMT phenotypes and aggressiveness of breast cancer. Here, we show that
Ets1
induces ZEB expression
and activates the ZEB1 promoter, independently of its threonine 38 phosphorylation status. In the basal-like subtype of breast cancer
cells, siRNAs targeting
Ets1
repressed expression of ZEBs and partially restored their epithelial phenotypes and sensitivity to anti-tumor drugs.
ESE1
, a member of the Ets transcription factor family, was originally characterized as being expressed in an epithelial-restricted pattern, placing it within the epithelium-specific ETS subfamily.
ESE1
, highly expressed in the luminal subtype of breast
cancer cells, was repressed by activation of MEK-ERK pathway, resulting in induction of ZEBs through
Ets1
upregulation. Conversely,
Est1, highly expressed in the basal-like subtype, was repressed by inactivation of MEK-ERK pathway, resulting in reduction of ZEBs
through
ESE1
upregulation. These findings suggest that
ESE1
and
Ets1
, whose expressions are reciprocally regulated by MEK-ERK
pathway, define the EMT phenotype through controlling expression of ZEBs in each subtype of breast cancer cells.
Biography
Nguyen Duy Sinh has 20 years of experience in treatment of cancer patients, he was awarded Ph.D. from University of Yamanashi, Japan and his research interests include
radiotherapy, progression of progression of epithelial tumors.
drsinh36@gmail.comNguyen Duy Sinh et al., Breast Can Curr Res 2017, 2:5 (Suppl)
DOI: 10.4172/2572-4118-C1-011