Gamze Nur Öter1, Merve Nur Işık Kolukısaoğlu2, İlknur Bingül2, Servet Tunoğlu3, Canan Küçükgergin2

1Department of Medical Biochemistry, İstanbul University, Institute of Health Sciences, İstanbul, Türkiye
2Department of Medical Biochemistry, İstanbul University, Faculty of Medicine, İstanbul, Türkiye
3Department of Medical Biology and Genetic, Demiroğlu Science University, Faculty of Medicine, İstanbul, Türkiye

Keywords: Epithelial-mesenchymal transition, PNT1A, prostate cancer, ZEB1, ZEB1-AS1.

Abstract

Objectives: Our purpose was to evaluate the expression of long non-coding RNA (lncRNA) zinc finger E-box binding homeobox 1-antisense 1 (ZEB1-AS1) and the transcription factor ZEB1 in prostate cancer (PCa) cells, and to explore their potential role in tumor aggressiveness and epithelial-mesenchymal transition (EMT) regulation.

Materials and methods: PC3, DU145, LNCaP, and PNT1A were cultured under standard conditions. miRNeasy Tissue/Cells Advanced Mini Kit was used to isolate total RNA. RT2 First Strand Kit was used to synthesize complementary DNA for lncRNAs, and miRCURY LNA RT Kit for microRNAs (miRNAs). Rotor-Gene Q (Qiagen) system was used to carry out quantitative real-time PCR (qRT-PCR) using SYBR Green chemistry. ZEB1-AS1 and ZEB1 levels were measured in the PCa in vitro model.

Results: The qRT-PCR analysis revealed that ZEB1-AS1 and ZEB1 were significantly upregulated in androgen-independent PC3 and DU145 cells compared with PNT1A (p<0.01), while LNCaP showed lower expression levels. Elevated ZEB1-AS1 was linked to higher ZEB1 expression, especially in PC3 cells, indicating EMT activation.

Conclusion: Our findings suggest the ZEB1-AS1/ZEB1 axis has a crucial role in PCa progression by promoting EMT and metastatic potential. This regulatory network could act as a possible marker and treatment goal, particularly in aggressive, androgen-independent PCa subtypes.

Cite this article as: Öter GN, Işık Kolukısaoğlu MN, Bingül İ, Tunoğlu S, Küçükgergin C. The ZEB1-AS1/ZEB1 axis promotes epithelial-mesenchymal transition in prostate cancer. D J Med Sci 2025;11(2):88-91. doi: 10.5606/fng. btd.2025.192.

Author Contributions

Conception/design of study, critical revision of manuscript, final approval and accountability: G.N.Ö.; Data acquisition, final approval and accountability: M.N.I.K.; Final approval and accountability, critical revision of manuscript: I.B.; Data analysis/interpretation, final approval and accountability: S.T.; Conception, critical revision of manuscript, final approval and accountability: C.K.

Conflict of Interest

The authors declared no conflicts of interest with respect to the authorship and/or publication of this article.

Financial Disclosure

The authors received no financial support for the research and/or authorship of this article.

Data Sharing Statement:
The data that support the findings of this study are available from the corresponding author upon reasonable request.