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Inositol polyphosphate 4-phosphatase type II regulation of androgen receptor activity
Manqi Zhang1, Egla Suarez2, Judy L Vasquez2
1Department of Chemistry and Biochemistry, Florida International University, Miami, FL, 33199, USA.
Oncogene
|September 20, 2018
Summary
Loss of INPP4B, a tumor suppressor, impacts androgen receptor (AR) activity and oncogenic signaling in prostate cancer. Restoring INPP4B may offer new therapeutic strategies for advanced prostate cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Androgen receptor (AR) signaling is crucial in prostate cancer progression.
- Loss of tumor suppressors INPP4B and PTEN is linked to AR activation in advanced prostate cancer.
- The role of INPP4B in AR regulation remains unclear.
Purpose of the Study:
- To investigate the role of INPP4B in regulating AR activity and associated signaling pathways.
- To determine if INPP4B loss contributes to AR-dependent transcriptional profiles in prostate cancer.
Main Methods:
- Utilized prostate cancer cell lines to assess INPP4B's effect on AR transcriptional activity, Akt, and PKC signaling.
- Analyzed gene expression data from prostate cancer patient cohorts.
- Employed an Inpp4b knockout (Inpp4b-/-) mouse model to study INPP4B's function in normal prostate tissue.
Main Results:
- INPP4B was found to regulate AR transcriptional activity, Akt, and PKC signaling in prostate cancer cells.
- A positive correlation was observed between INPP4B expression and AR mRNA levels/transcriptional output in patient cohorts.
- In Inpp4b-/- mice, INPP4B loss suppressed Akt and PKC signaling and modulated AR transcriptional activity without affecting PTEN levels.
Conclusions:
- INPP4B plays a significant role in modulating AR activity in normal prostate epithelium.
- Loss of INPP4B contributes to the AR-dependent transcriptional reprogramming observed in prostate cancer.
- INPP4B is a potential therapeutic target for managing advanced prostate cancer.
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