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Parallel Reporter Assays Identify Altered Regulatory Role of rs684232 in Leading to Prostate Cancer Predisposition
Naixia Ren1, Qingqing Liu1, Lingjie Yan1
1Shandong Provincial Key Laboratory of Animal Cell and Developmental Biology, School of Life Sciences, Shandong University, Qingdao 266237, China.
International Journal of Molecular Sciences
|August 27, 2021
Summary
Identifying regulatory single nucleotide polymorphisms (SNPs) linked to prostate cancer risk is crucial. This study found rs684232 alters gene expression, impacting cancer progression and offering potential for patient prognostics.
Area of Science:
- Genetics
- Oncology
- Molecular Biology
Background:
- Genome-wide association studies (GWAS) identify cancer risk-associated single nucleotide polymorphisms (SNPs), but functional characterization remains challenging.
- Understanding how these SNPs influence gene regulation is vital for elucidating cancer development and progression.
Purpose of the Study:
- To identify regulatory SNPs associated with prostate cancer risk that can cause transcriptional misregulation.
- To investigate the functional mechanism of a specific risk SNP, rs684232, in prostate cancer malignancy.
Main Methods:
- Parallel reporter gene assays were conducted using both alleles of 213 prostate cancer risk-associated GWAS SNPs in 22Rv1 cells.
- Chromatin immunoprecipitation and gene expression analysis were performed to assess the impact of rs684232 variation.
Main Results:
- Thirty-two regulatory SNPs demonstrating differential allelic activity were identified.
- The SNP rs684232 was shown to affect transcription factor FOXA1 binding, leading to altered expression of VPS53, FAM57A, and GEMIN4.
- These genes are implicated in prostate cancer malignancy.
Conclusions:
- The study elucidates the role and mechanism of rs684232 in prostate cancer progression.
- Findings suggest rs684232 can serve as a prognostic marker and a potential therapeutic target for prostate cancer.
