Oncogenic ACSM1 in prostate cancer is through metabolic and extracellular matrix-receptor interaction signaling

Yongchen Guo1, Chunna Ren2, Wentao Huang3

  • 1Department of Immunology, Mudanjiang Medical University Mudanjiang 157011, China.

Insights

Acyl-coenzyme A synthetase medium chain family member 1 (ACSM1) is elevated in prostate cancer, driving oncogenic roles through metabolic and ECM-receptor pathways. Its amplification correlates with metastasis and poorer survival, suggesting ACSM1 as a potential biomarker and therapeutic target.

Area of Science:

  • Molecular oncology
  • Cancer metabolism
  • Prostate cancer research

Background:

  • Acyl-coenzyme A synthetase medium chain family member 1 (ACSM1) is involved in fatty acid metabolism.
  • The oncogenic role of ACSM1 in cancer, particularly prostate cancer, is not well understood.

Purpose of the Study:

  • To investigate the role of ACSM1 in prostate cancer development and progression.
  • To determine if ACSM1 expression or genetic alterations correlate with clinical outcomes in prostate cancer patients.

Main Methods:

  • Analysis of gene expression profiles and genomic datasets.
  • Gene function stratification and gene set enrichment analysis.
  • Correlation analysis between ACSM1 alterations and clinical parameters like metastasis and survival.

Main Results:

  • ACSM1 expression is significantly increased in prostate cancer tissues compared to non-tumor tissues.
  • Increased ACSM1 expression and gene amplifications are associated with poor prognosis, metastasis, and reduced survival.
  • ACSM1's oncogenic functions are linked to metabolic and extracellular matrix (ECM)-receptor interaction pathways, independent of immune signaling.

Conclusions:

  • ACSM1 is a potential oncogene in prostate cancer, with elevated expression and amplification linked to adverse clinical outcomes.
  • ACSM1 may serve as a valuable biomarker for prostate cancer screening and prognosis.
  • Targeting ACSM1 could offer a novel therapeutic strategy for prostate cancer.

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