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This study identified key genes in HCC development with emphasis on mitochondrial dysfunction and apoptosis. Methods: Differential expression across TCGA-LIHC, GSE36076, and GSE95698 defined overlapping DEGs, followed by a six-gene prognostic risk model. CSRNP1 expression in HCC cells was assessed by WB and qRT-PCR, while proliferation, migration, apoptosis, ROS (cytoplasmic and mitochondrial), and JNK/p38 activation were evaluated using standard functional and imaging assays. Results: CSRNP1 knockdown increased proliferation and reduced apoptosis; overexpression disrupted mitochondrial integrity, raised ROS, and activated JNK/p38 MAPK; NAC or SP600125 attenuated these effects. 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Email: [lukaiehbh@163.com](lukaiehbh@163.com); Wenchao Wang. Email: [wangwenchaosmmu@163.com](wangwenchaosmmu@163.com);\u003Cbr>Maoling Zhu. Email: [zlcg1984@163.com](zlcg1984@163.com)\u003Cbr>\\# These authors contributed equally to this work\u003Cbr>§ The primary corresponding author\u003Cbr>Received: 05 June 2025; Accepted: 03 September 2025; Published: 30 December 2025\u003Cbr>ABSTRACT: Background: Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related mortality worldwide. This study aimed to identify key genes involved in HCC development and elucidate their molecular mechanisms, with a particular focus on mitochondrial function and apoptosis. Methods: Differential expression analyses were performed across three datasets—The Cancer Genome Atlas (TCGA)-Liver Hepatocellular Carcinoma (LIHC), GSE36076, and GSE95698—to identify overlapping differentially expressed genes (DEGs) . A prognostic risk model was then constructed. Cysteine/serine-rich nuclear protein 1 (CSRNP1)expression levels inHCC cell lines were assessed via western blot (WB) and quantitative reverse transcription polymerase chain reaction (qRT-PCR) . The effects of CSRNP1 knockdown or overexpression on cell proliferation, migration, and apoptosis were evaluated using cell counting-8 (CCK-8) assays, Transwell assays, and flow cytometry. Mitochondrial ultrastructure was examined by transmission electron microscopy, and intracellular and mitochondrial reactive oxygen species (mROS) levels were measured using specific fluorescent probes. WB was used to assess activation of the c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK) pathway, and pathway dependence was examined using the ROS scavenger N-Acetylcysteine (NAC) and the JNK inhibitor SP600125 . Results: A six-gene prognostic model was established, comprising downregulated genes (NR4A1 and CSRNP1) and upregulated genes (CENPQ, YAE1, FANCF, and POC5) in HCC. Functional experiments revealed that CSRNP1 knockdown promoted the proliferation of HCC cells and suppressed their apoptosis. Conversely, CSRNP1 overexpression impaired mitochondrial integrity, increased both mitochondrial and cytoplasmic ROS levels, and activated the JNK/p38 MAPK pathway. Notably, treatment with NACor SP600125 attenuated CSRNP1-induced MAPK activation and apoptosis. Conclusion: CSRNP1 is a novel prognostic biomarker and tumor suppressor in HCC. It exerts anti-tumor effects by inducing oxidative stress and activating the JNK/p38 MAPK pathway in a ROS-dependent manner. These findings suggest that CSRNP1 may serve as a potential therapeutic target in the management of HCC.\u003Cbr>KEYWORDS: Cysteine/serine-rich nuclear protein 1; c-Jun N-terminal kinase/p38 mitogen-activated protein kinase pathway; hepatocellular carcinoma; reactive oxygen species accumulation; mitochondrial dysfunction |  |\n\nCopyright © 2026 The Authors. Published by Tech Science Press.  \nThis work is licensed under a Creative Commons Attribution 4.0 Int","cbCaifStZcd5udQL","https://ap.wps.com/l/cbCaifStZcd5udQL","pdf",34384541,21,"English","# Abstract\n# Keywords\n# 1 Introduction","[{\"question\":\"What was the primary research goal of this study on hepatocellular carcinoma?\",\"answer\":\"To identify key genes involved in HCC development and clarify their molecular mechanisms, focusing on mitochondrial function and apoptosis.\"},{\"question\":\"How did CSRNP1 manipulation affect HCC cell behavior?\",\"answer\":\"CSRNP1 knockdown promoted HCC cell proliferation and suppressed apoptosis, whereas CSRNP1 overexpression impaired mitochondrial integrity, increased ROS, and enhanced JNK/p38 MAPK pathway activation.\"},{\"question\":\"Why were NAC and SP600125 used, and what did they show?\",\"answer\":\"They were used to test pathway dependence; both attenuated CSRNP1-induced MAPK activation and apoptosis, supporting a ROS-dependent mechanism.\"}]","CSRNP1 Promotes Apoptosis and Mitochondrial Dysfunction via ROS-Mediated JNK/p38 MAPK Pathway Activation in Hepatocellular Carcinoma | PDF",1790711285,53]