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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