Open Access

ARTICLE

3-Hydroxysterol Δ24-Reductase Promotes Ovarian Cancer Progression by Activating the TGF-1/Smad2/3 Signaling Pathway

Wenjing Liao^1,#, Liaodi Wang^2,#, Zhen Huang¹, Ziyu Zou¹, Yimin Liu¹, Haoyue Liu¹, Zhaoning Duan¹, Liangdan Tang^1,*

1 Department of Gynecology and Obstetrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China
2 Department of Radiology, Ping An Healthcare Diagnostics Center, Wuhan, 430014, China

* Corresponding Author: Liangdan Tang. Email:
# These authors contributed equally to this work

(This article belongs to the Special Issue: Identification of potential targets and biomarkers for cancers and the exploration of novel molecular mechanisms of tumorigenesis and metastasis)

Oncology Research 2025, 33(10), 3041-3064. https://doi.org/10.32604/or.2025.065451

Received 13 March 2025; Accepted 15 May 2025; Issue published 26 September 2025

Abstract

Objectives: Ovarian cancer (OC) is a highly heterogeneous disease characterized by high metastatic potential and frequent recurrence. 3β-hydroxysterol Δ24-reductase (DHCR24) is closely associated with the progression of various malignant tumors, but its role in OC remains unexplored. This study is the first to systematically investigate the function of DHCR24 in OC and elucidate its mechanism in promoting OC progression, providing novel theoretical insights for targeted therapy. Methods: The expression of DHCR24 was evaluated in tissues using bioinformatics and clinical data; the impact of DHCR24 on the malignant behavior of OC was assessed through in vivo and in vitro experiments; and the mechanism by which DHCR24 functions in OC was preliminarily explored using sequencing and rescue experiments. Statistical analysis was conducted using the chi-square test, t-test, and one-way ANOVA. Results: Database, clinical data, and immunohistochemical (IHC) analyses demonstrated that DHCR24 is upregulated in OC and correlates with poor outcomes. In vitro experiments indicated that DHCR24 promotes proliferation, migration, invasion, and epithelial-mesenchymal transition in OC cells. The addition of a DHCR24 inhibitor suppressed the malignant behavior of OC cells. The nude mouse tumor formation experiment demonstrated that inhibiting DHCR24 suppresses the in vivo growth of OC cells. Further experiments showed that DHCR24 promotes the malignant behavior of OC cells, correlating with the regulation of the transforming growth factor beta (TGF-β) signaling pathway. All the above experiments showed statistical significance. Conclusion: DHCR24 contributes to ovarian cancer progression by upregulating the TGF-β1 pathway, highlighting its potential as a therapeutic target in ovarian cancer.

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Supplementary Material

Supplementary Material File

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