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Updated: Dec 14, 2025
11:29
miRNA Expression Analyses in Prostate Cancer Clinical Tissues
Published on: September 8, 2015
11.1K
Increased nuclear factor I/B expression in prostate cancer correlates with AR expression.
Jagpreet S Nanda1,2, Wisam N Awadallah1,2, Sarah E Kohrt2,3
1Department of Urology, Case Western Reserve University, Cleveland, Ohio.
The Prostate
|July 22, 2020
Summary
Nuclear factor I/B (NFIB) expression increases in prostate cancer and interacts with the androgen receptor (AR). NFIB levels predict recurrence, especially in castration-resistant prostate cancer, highlighting its role in prostate cancer progression.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Prostate cancer often expresses androgen receptor (AR), a key therapeutic target.
- Nuclear factor I/B (NFIB) has been shown to regulate AR activity in prostate cancer cells.
- The expression and role of NFIB in clinical prostate cancer samples were previously unknown.
Purpose of the Study:
- To investigate the expression patterns of NFIB in various stages of prostate cancer.
- To determine the correlation between NFIB expression, AR activity, and neuroendocrine prostate cancer (NEPCa) markers.
- To elucidate the interaction between NFIB and AR in prostate cancer.
Main Methods:
- Immunohistochemical staining of NFIB, AR, and synaptophysin on prostate cancer tissue microarrays.
- Analysis of public datasets (cBioPortal) for NFIB, AR, and NEPCa activity scores.
- Western blot analysis and subcellular fractionation of prostate cancer cell lines for NFIB expression and localization.
- Co-immunoprecipitation assays to assess NFIB-AR interaction.
Main Results:
- NFIB expression increased in prostate cancer tissues compared to normal controls, localized to both nucleus and cytoplasm.
- Cytoplasmic AR and synaptophysin increased in primary prostate cancer; NFIB was highly expressed in small cell prostate cancer.
- The ratio of cytoplasmic-to-nuclear NFIB predicted earlier biochemical recurrence, and cytoplasmic AR was an independent predictor.
- NFIB expression correlated positively with AR activity and negatively with NEPCa score in castration-resistant prostate cancer.
- NFIB and AR were found to interact via co-immunoprecipitation.
Conclusions:
- NFIB is differentially expressed in prostate cancer, with altered localization in castration-resistant disease.
- NFIB expression and localization are associated with AR activity and clinical outcomes, including recurrence.
- A direct interaction between NFIB and AR was confirmed, suggesting a functional link in prostate cancer progression.
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