Authors :
Madhab Mondal; Prerna Rai; Akash Baglari; Divyadarshi Rai; Pratiksha Chhetri; Purandar Sarkar
Volume/Issue :
Volume 10 - 2025, Issue 9 - September
Google Scholar :
https://tinyurl.com/yw8ncrjk
Scribd :
https://tinyurl.com/565h88z5
DOI :
https://doi.org/10.38124/ijisrt/25sep352
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Abstract :
Prostate cancer (PCa) progression is primarily driven by androgen receptor (AR) signaling, which orchestrates
tumor proliferation and metabolic reprogramming. Alpha-Methyl Acyl-CoA Racemase (AMACR) is a key enzyme in
branched-chain fatty acid β-oxidation which is widely recognized as a diagnostic marker for PCa but its regulatory
association with AR and functional implications remain unclear. Using globally available multi-omics datasets, we analyzed
RNA-seq profiles from TCGA-PRAD which revealed significant overexpression of AMACR in tumors compared to normal
tissues (p < 0.001). Elevated AMACR levels correlated with advanced Gleason scores, nodal positivity, and poor overall
survival (p = 0.027). Functional insights from androgen stimulation and antagonism datasets, along with Chipset analyses,
demonstrated direct AR occupancy at enhasssncer regions near AMACR which further confirms androgen-dependent
transcriptional regulation. Protein-level evidence from immunohistochemistry and immunofluorescence supported these
findings. Collectively, these results establish AMACR as an AR-regulated biomarker in PCa, implicating it in metabolic
dysregulation and disease aggressiveness, and highlight its potential as a therapeutic target within the androgen-driven
oncogenic network.
Keywords :
Prostate cancer, AMACR, Androgen receptor, Biomarker.
References :
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- Aurilio G, Cimadamore A, Mazzucchelli R, et al. Androgen Receptor Signaling Pathway in Prostate Cancer: From Genetics to Clinical Applications. Cells 2020; 9: 2653.
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Prostate cancer (PCa) progression is primarily driven by androgen receptor (AR) signaling, which orchestrates
tumor proliferation and metabolic reprogramming. Alpha-Methyl Acyl-CoA Racemase (AMACR) is a key enzyme in
branched-chain fatty acid β-oxidation which is widely recognized as a diagnostic marker for PCa but its regulatory
association with AR and functional implications remain unclear. Using globally available multi-omics datasets, we analyzed
RNA-seq profiles from TCGA-PRAD which revealed significant overexpression of AMACR in tumors compared to normal
tissues (p < 0.001). Elevated AMACR levels correlated with advanced Gleason scores, nodal positivity, and poor overall
survival (p = 0.027). Functional insights from androgen stimulation and antagonism datasets, along with Chipset analyses,
demonstrated direct AR occupancy at enhasssncer regions near AMACR which further confirms androgen-dependent
transcriptional regulation. Protein-level evidence from immunohistochemistry and immunofluorescence supported these
findings. Collectively, these results establish AMACR as an AR-regulated biomarker in PCa, implicating it in metabolic
dysregulation and disease aggressiveness, and highlight its potential as a therapeutic target within the androgen-driven
oncogenic network.
Keywords :
Prostate cancer, AMACR, Androgen receptor, Biomarker.