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Updated: Jun 10, 2026
miRNA Expression Analyses in Prostate Cancer Clinical Tissues
Published on: September 8, 2015
Expression and function of ATIP/MTUS1 in human prostate cancer cell lines
Simon N S Louis1, Laurie Chow, Linda Rezmann
1Clinical Pharmacology and Therapeutics Unit, University of Melbourne, Department of Medicine, Austin Health, Heidelberg, Victoria, Australia.
Background:
We have previously demonstrated Ang II type 2 (AT(2)-) receptor-mediated inhibition of EGF-induced prostate cancer cell growth in androgen-dependent (LNCaP) and independent (PC3) prostate cancer cell lines.
Methods:
To explore the signaling pathways involved in this inhibitory effect, we examined the interaction of the AT(2)-receptor with its novel regulatory partner ATIP using real time PCR, over-expression, siRNA and [(3)H]thymidine incorporation assays.
Results:
The results in human prostate cancer cell lines demonstrate the presence of ATIP in both cell lines examined, and suggest that (i) the AT(2)-receptor through an interaction with ATIP mediates an anti-growth factor effect in both androgen-dependent and androgen-independent cell lines; (ii) ATIP expression decreases as the rate of cell growth and androgen-independence increase; and (iii) EGF may act on cell growth in part by reducing the content of ATIP present in the cells.
Conclusions:
The results support our earlier proposal in normal cell lines that ATIP is an important component of the cellular response to AT(2)-receptor activation. The results further suggest that a critical level of ATIP is required to mediate the effect of AT(2)-receptor activation to inhibit EGF mediated increases in cell growth. They also suggest that EGF may in part induce cell growth by suppressing the level of ATIP expression.
Insights
The Angiotensin II type 2 (AT(2)) receptor, through its partner ATIP, inhibits prostate cancer cell growth. EGF may promote growth by reducing ATIP levels, highlighting ATIP's role in AT(2)-receptor-mediated anti-growth effects.
Area of Science:
- Oncology
- Molecular Biology
- Endocrinology
Background:
- Previously demonstrated AT(2)-receptor-mediated inhibition of EGF-induced prostate cancer cell growth.
- Studied androgen-dependent (LNCaP) and independent (PC3) prostate cancer cell lines.
Purpose of the Study:
- Explore signaling pathways in AT(2)-receptor-mediated inhibition of prostate cancer cell growth.
- Examine the interaction between AT(2)-receptor and its novel partner ATIP.
Main Methods:
- Real-time PCR
- Over-expression assays
- siRNA
- [(3)H]thymidine incorporation assays.
Main Results:
- Confirmed ATIP presence in both LNCaP and PC3 cell lines.
- AT(2)-receptor/ATIP interaction mediates anti-growth effects in both cell types.
- Decreased ATIP expression correlated with increased cell growth and androgen-independence.
- EGF may stimulate cell growth by reducing cellular ATIP content.
Conclusions:
- ATIP is crucial for the cellular response to AT(2)-receptor activation.
- Sufficient ATIP levels are required for AT(2)-receptor to inhibit EGF-mediated growth.
- EGF may induce prostate cancer cell growth by suppressing ATIP expression.
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