ORIGINAL RESEARCH article
Front. Oncol.
Sec. Cancer Immunity and Immunotherapy
Volume 15 - 2025 | doi: 10.3389/fonc.2025.1619123
This article is part of the Research TopicAdvancing Non-small Lung Cancer Management Through Biomarker IntegrationView all 3 articles
CCDC58 drives lung adenocarcinoma progression via the PI3K/AKT signaling pathway
Provisionally accepted
Wenchao Dai1,2
Jun Yang1,2
Wenming Yang3
Guibin Zhang1Hang Chen1Bi Ren1Xin Dang1Linfeng Xue1Li Jiang1,2*- 1North Sichuan Medical College, Nanchong, China
- 2Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan Province, China
- 3West China Second University Hospital, Sichuan University, Chengdu, Sichuan Province, China
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Background: Previous studies have implicated Coiled-coil domain-containing 58 (CCDC58) in the malignant progression of hepatocellular carcinoma and breast cancer. However, its role in lung adenocarcinoma (LUAD) remains poorly understood.Methods: Bioinformatics analysis was employed to examine CCDC58 expression patterns in LUAD and their correlation with clinical features. We validated CCDC58 expression levels using quantitative real-time PCR (qPCR), Western Blot (WB), and immunohistochemistry staining (IHC). Furthermore, we assessed the impact of CCDC58 knockdown on LUAD cell behavior using proliferation assays, cell migration assays, wound healing assays, and flow cytometry. We explored the effects of CCDC58 knockdown on apoptotic proteins, epithelial-mesenchymal transition (EMT) markers, and PI3K/AKT signaling pathway components through WB. Finally, we evaluated the role of CCDC58 in tumor growth in vivo using a nude mouse xenograft model, with subsequent IHC analysis of tumor tissues.Results: CCDC58 showed significant upregulation in LUAD cell lines and clinical specimens, leading to poor prognosis. CCDC58 expression was identified significant correlation with tumor microenvironment. In vitro, suppressing CCDC58 expression significantly impaired the capacity of growth and migration of LUAD cells. CCDC58 knockdown inhibited EMT, promoted apoptosis, and induced G1-phase cell cycle arrest. Significantly, CCDC58 knockdown inhibited the activity of the PI3K/AKT signaling pathway. In vivo, CCDC58 knockdown suppressed tumor growth and enhanced apoptosis.Conclusions: Above all, this study reveals that CCDC58 plays multiple pro-tumorigenic roles in the progression of LUAD. These results enhance the understanding of LUAD pathogenesis and highlight CCDC58 as a potential therapeutic target and prognostic biomarker.
Keywords: CCDC58, PI3K/Akt signaling pathway, EMT, LUAD；cell proliferation, Apoptosis 1. Introduction
Received: 27 Apr 2025; Accepted: 22 Aug 2025.
Copyright: © 2025 Dai, Yang, Yang, Zhang, Chen, Ren, Dang, Xue and Jiang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Li Jiang, North Sichuan Medical College, Nanchong, China
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