1. Academic Validation
  2. Long non-coding RNA PRSS23-AS1 as ceRNA promotes breast cancer progression by regulating EMT via miR-3176 /YBX1 axis

Long non-coding RNA PRSS23-AS1 as ceRNA promotes breast cancer progression by regulating EMT via miR-3176 /YBX1 axis

  • Cancer Gene Ther. 2025 Sep;32(9):1018-1029. doi: 10.1038/s41417-025-00943-3.
Yun Huang # 1 Mudan Feng # 2 Yiwei Jiang # 1 3 Maihuan Wang 4 Mingkun Wang 5 Zhen Cao 6 7 8
Affiliations

Affiliations

  • 1 Department of General Surgery, The Sixth Medical Center, Chinese PLA General Hospital, Beijing, China.
  • 2 Department of Emergency, The Seventh Medical Centre, Chinese PLA General Hospital, Beijing, China.
  • 3 Department of General Surgery, School of Medicine, South China University of Technology, Guangzhou, China.
  • 4 Department of General Surgery, The First Medical Centre, Chinese PLA General Hospital, Beijing, China.
  • 5 Department of General Surgery, The Sixth Medical Center, Chinese PLA General Hospital, Beijing, China. wangmingkun@301hospital.com.cn.
  • 6 Department of General Surgery, The Sixth Medical Center, Chinese PLA General Hospital, Beijing, China. caozhen@301hospital.com.cn.
  • 7 Department of General Surgery, School of Medicine, South China University of Technology, Guangzhou, China. caozhen@301hospital.com.cn.
  • 8 Department of General Surgery, The First Medical Centre, Chinese PLA General Hospital, Beijing, China. caozhen@301hospital.com.cn.
  • # Contributed equally.
Abstract

Breast Cancer (BC) remains a leading cause of cancer-related mortality, largely due to its aggressive proliferation and metastatic potential. Long non-coding RNAs (lncRNAs) have emerged as key regulators in tumor development and progression. This study explored the functional role and mechanism of Lnc-PRSS23-AS1 in BC. We assessed Lnc-PRSS23-AS1 expression and localization using fluorescence in situ hybridization, qRT-PCR, and Western blotting in BC tissues and cell lines. Binding interactions between Lnc-PRSS23-AS1, miR-3176, and Y-box binding protein 1 (YBX1) were validated through dual-luciferase reporter assays, RNA pulldown, and RNA immunoprecipitation. Lnc-PRSS23-AS1 was significantly upregulated in BC and predominantly localized in the cytoplasm. Silencing Lnc-PRSS23-AS1 or overexpressing miR-3176 suppressed BC cell proliferation, migration, and invasion in vitro and in vivo. Conversely, miR-3176 inhibition or YBX1 overexpression reversed these effects. Mechanistically, Lnc-PRSS23-AS1 promoted YBX1 protein expression by acting as a molecular Sponge for miR-3176. These findings highlight the Lnc-PRSS23-AS1/miR-3176/YBX1 axis as a driver of BC progression and suggest Lnc-PRSS23-AS1 as a potential therapeutic target for breast Cancer treatment.

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