Regulation of gene expression by the androgen receptor and hedgehog pathways in breast cancer cells

Vivian Yar Li Chua

Regulation of gene expression by the androgen receptor and hedgehog pathways in breast cancer cells

Vivian Yar Li Chua

Research output: Thesis › Doctoral Thesis

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Abstract

[Truncated] The androgen receptor (AR) is expressed in 70-90% of breast tumours and its increased

expression in oestrogen receptor (ER) expressing breast cancers is correlated with better disease
prognosis and longer relapse-free and overall survival. The Hedgehog signalling pathway has also
been implicated in breast cancer growth, with Hedgehog signalling intermediates and
Hedgehog-induced target genes overexpressed in both early stage and aggressive breast tumours. The
androgen, 5α-dihydrotestosterone (DHT) and the Hedgehog pathway inhibitor, cyclopamine, inhibit
proliferation of the MCF-7 and T- 47D breast cancer cell lines and this thesis has investigated
genes and cellular processes regulated by these agents that would potentially impede breast tumour
progression. In DHT and cyclopamine treated MCF-7 and T-47D cells, screening of gene expression
using RT2 Profiler Human Breast Cancer PCR Arrays identified decreased expression of

both the ABC transporters, ABCB1 and ABCG2, which facilitate the development of drug resistance in
cancer cells, and regulators of epithelial-to-mesenchymal transition (EMT), a program associated
with induction of cancer cell motility, invasiveness and metastasis.

Original language	English
Qualification	Doctor of Philosophy
Supervisors/Advisors	Yeap, Bu, Supervisor Harvey, Jennet, Supervisor Bentel, Jacqueline, Supervisor
Publication status	Unpublished - 2015

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SDG 3 Good Health and Well-being

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@phdthesis{94b881dbd2704195a467addeb2fa8f80,

title = "Regulation of gene expression by the androgen receptor and hedgehog pathways in breast cancer cells",

abstract = "[Truncated] The androgen receptor (AR) is expressed in 70-90\% of breast tumours and its increasedexpression in oestrogen receptor (ER) expressing breast cancers is correlated with better disease prognosis and longer relapse-free and overall survival. The Hedgehog signalling pathway has also been implicated in breast cancer growth, with Hedgehog signalling intermediates and Hedgehog-induced target genes overexpressed in both early stage and aggressive breast tumours. The androgen, 5α-dihydrotestosterone (DHT) and the Hedgehog pathway inhibitor, cyclopamine, inhibit proliferation of the MCF-7 and T- 47D breast cancer cell lines and this thesis has investigated genes and cellular processes regulated by these agents that would potentially impede breast tumour progression. In DHT and cyclopamine treated MCF-7 and T-47D cells, screening of gene expression using RT2 Profiler Human Breast Cancer PCR Arrays identified decreased expression ofboth the ABC transporters, ABCB1 and ABCG2, which facilitate the development of drug resistance in cancer cells, and regulators of epithelial-to-mesenchymal transition (EMT), a program associated with induction of cancer cell motility, invasiveness and metastasis. ",

keywords = "Breast cancer, Hedgehog pathway, EMT, Androgen receptor, ABCG2 drug transporter",

author = "Chua, \{Vivian Yar Li\}",

year = "2015",

language = "English",

}

TY - BOOK

T1 - Regulation of gene expression by the androgen receptor and hedgehog pathways in breast cancer cells

AU - Chua, Vivian Yar Li

PY - 2015

Y1 - 2015

N2 - [Truncated] The androgen receptor (AR) is expressed in 70-90% of breast tumours and its increasedexpression in oestrogen receptor (ER) expressing breast cancers is correlated with better disease prognosis and longer relapse-free and overall survival. The Hedgehog signalling pathway has also been implicated in breast cancer growth, with Hedgehog signalling intermediates and Hedgehog-induced target genes overexpressed in both early stage and aggressive breast tumours. The androgen, 5α-dihydrotestosterone (DHT) and the Hedgehog pathway inhibitor, cyclopamine, inhibit proliferation of the MCF-7 and T- 47D breast cancer cell lines and this thesis has investigated genes and cellular processes regulated by these agents that would potentially impede breast tumour progression. In DHT and cyclopamine treated MCF-7 and T-47D cells, screening of gene expression using RT2 Profiler Human Breast Cancer PCR Arrays identified decreased expression ofboth the ABC transporters, ABCB1 and ABCG2, which facilitate the development of drug resistance in cancer cells, and regulators of epithelial-to-mesenchymal transition (EMT), a program associated with induction of cancer cell motility, invasiveness and metastasis.

AB - [Truncated] The androgen receptor (AR) is expressed in 70-90% of breast tumours and its increasedexpression in oestrogen receptor (ER) expressing breast cancers is correlated with better disease prognosis and longer relapse-free and overall survival. The Hedgehog signalling pathway has also been implicated in breast cancer growth, with Hedgehog signalling intermediates and Hedgehog-induced target genes overexpressed in both early stage and aggressive breast tumours. The androgen, 5α-dihydrotestosterone (DHT) and the Hedgehog pathway inhibitor, cyclopamine, inhibit proliferation of the MCF-7 and T- 47D breast cancer cell lines and this thesis has investigated genes and cellular processes regulated by these agents that would potentially impede breast tumour progression. In DHT and cyclopamine treated MCF-7 and T-47D cells, screening of gene expression using RT2 Profiler Human Breast Cancer PCR Arrays identified decreased expression ofboth the ABC transporters, ABCB1 and ABCG2, which facilitate the development of drug resistance in cancer cells, and regulators of epithelial-to-mesenchymal transition (EMT), a program associated with induction of cancer cell motility, invasiveness and metastasis.

KW - Breast cancer

KW - Hedgehog pathway

KW - EMT

KW - Androgen receptor

KW - ABCG2 drug transporter

M3 - Doctoral Thesis

ER -

Regulation of gene expression by the androgen receptor and hedgehog pathways in breast cancer cells

Abstract

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