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academies
Cell Science, Stem Cell Research &
Pharmacological Regenerative Medicine
November 29-30, 2017 | Atlanta, USA
Annual Congress on
Adv cel sci tissue cul 2017 | Volume 1 Issue 2
ID4 regulates prostate development and stem cell population in mice prostate
Jaideep Chaudhary, Dhanushka Hewa Bostanthirige, Jugal Joshi, Shravan Kumar
and
Divya Patel
Clark Atlanta University, USA
I
nhibitor of differentiation 4 (Id4), a member of the helix-
loop-helix family of transcriptional regulators is a novel
prostate cancer (PCa) tumor suppressor. Recent studies have
shown that Id4 is highly expressed in the normal prostate
and decreases in prostate cancer (PCa) due to epigenetic
silencing. Genetic ablation of Id (Id4-/-) in mice leads to
underdeveloped prostate without the loss of Androgen
Receptor (AR) expression but with re-directed activity.
In this study, we demonstrate that prostates from the Id4
knockout (Id4-/-) mice show hyperplasia associated with
increased stem cell population that was evident by increased
Sca-1 and p63 expression. Histological analyses of adult
Id4-/- mice prostate shows increased Amacr expression, a
biomarker for early prostatic epithelial neoplasia (PIN) but
without a clear evidence of PCa. Immuno-histochemical
analysis demonstrated undetectable Nkx3.1 and Pten tumor
suppressors suggesting lack of epithelial differentiation.
Although Pten protein was not present in Id4-/- mice, the
presence of the corresponding Pten mRNA suggested intact
transcription of the gene with a possible translational or
post-translation defect. These results suggested that Id4
plays a role in regulating the translation of the Pten mRNA.
The results suggested that Id4-/- results in PIN lesions that
may be in part due to a block in Pten translation. These data
suggest that loss of Id4 can initiate PIN like lesions through
multiple mechanisms such as by maintaining stemness (Sca-
1) and down-regulating known tumor suppressors (Pten)
and promoters of epithelial differentiation (Nkx3.1) while
having no effect on AR expression and function that is
reminiscent of castration resistant prostate cancer. We are
currently investigating the possible mechanisms by which
Id4 regulates cell fate and translational/post-translational
mechanisms involved in the regulation Pten.
Speaker Biography
Jaideep Chaudhary has his expertise in Bioinformatics and Molecular Biology. He uses
large datasets (microarray and NGS) to develop molecular pathways involved in cell
differentiation and diseases, primarily cancer. He is passionate about teaching and
mentoring Undergraduate and Graduate students. As a Scientist and an Administrator,
he works across the aisle to create educational programs that help developing the new
generation of productive scientists and educators.
e:
jchaudhary@cau.edu