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PRAME-AS lncRNA, regulated by MZF1, modulates PRAME expression and cell stemness
Zahra Hosseininia1,2, Hesam Dehghani1,2,3
1Division of Biotechnology, Faculty of Veterinary Medicine, Ferdowsi University of Mashhad, Mashhad, Iran.
Plos One
|September 17, 2025
Summary
The PRAME-AS long non-coding RNA regulates PRAME gene expression. Its knockout reduces PRAME levels and impacts cancer cell growth, migration, and viability, with MZF1 and DNA methylation influencing both genes.
Area of Science:
- Molecular Biology
- Cancer Research
- Epigenetics
Background:
- PRAME is a cancer-testis antigen (CTA) primarily expressed in testes, but also in some normal tissues like the endometrium.
- The regulatory mechanisms of PRAME, particularly the role of long non-coding RNAs (lncRNAs), are not well understood.
- Understanding PRAME regulation is crucial due to its tumor-restricted expression.
Purpose of the Study:
- To investigate the role of PRAME-AS lncRNA in regulating PRAME expression.
- To determine the effects of PRAME-AS ablation on cancer cell characteristics.
- To explore the influence of MZF1 and DNA methylation on PRAME and PRAME-AS expression.
Main Methods:
- PRAME-AS gene knockout and assessment of PRAME expression and cellular functions.
- Manipulation of PRAME-AS expression via MZF1 overexpression and upstream region hypermethylation.
- EGFP reporter assay to evaluate the regulatory region's ability to drive PRAME-AS transcription.
Main Results:
- PRAME-AS knockout decreased PRAME transcript levels by ~37% and reduced cell migration, proliferation, stemness, and viability.
- MZF1 overexpression increased PRAME expression ~2-fold and PRAME-AS levels >3-fold.
- Hypermethylation of the PRAME-AS upstream region reduced PRAME transcripts by ~50% and PRAME-AS levels by 18.5%.
Conclusions:
- PRAME-AS lncRNA acts as a key regulator of PRAME transcript levels.
- MZF1 and DNA methylation status of a shared CpG island influence the expression of both PRAME and PRAME-AS.
- The PRAME locus regulatory region alone is insufficient to drive PRAME-AS transcription in the antisense direction.
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