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已发表论文
Cms1 核糖体小亚基同源物通过调节 TNF/NF-κB 信号通路促进肝细胞癌的增殖和迁移
Authors Zhang T, Huang Y, Hu S, Yu Y, Qin F, Zhang Y, Cai Z, Wang H, Zhang P, Dai J
Received 23 June 2025
Accepted for publication 10 October 2025
Published 28 October 2025 Volume 2025:12 Pages 2429—2443
DOI https://doi.org/10.2147/JHC.S549003
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Prof. Dr. Imam Waked
Tuo Zhang,1,* Yongping Huang,2,* Sha Hu,2 Yongjie Yu,2 Fang Qin,2 Yu Zhang,2 Zeming Cai,3 Haitao Wang,2 Peng Zhang,2 Jing Dai1,4
1Department of Radiation and Medical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 430071, People’s Republic of China; 2Wuhan University Taikang Medical School (School of Basic Medical Sciences), Wuhan, Hubei, 430071, People’s Republic of China; 3Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, People’s Republic of China; 4Hubei Key Laboratory of Tumor Biological Behaviors, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 430071, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Jing Dai, Department of Radiation and Medical Oncology, Zhongnan Hospital of Wuhan University, 169 East Lake Road, Wuchang District, Wuhan, Hubei, 430071, People’s Republic of China, Email daijing@znhospital.cn Peng Zhang, Wuhan University Taikang Medical School (School of Basic Medical Sciences), 115 East Lake Road, Wuchang District, Wuhan, Hubei, 430071, People’s Republic of China, Email zhp@whu.edu.cn
Purpose: The study aims to further classify hepatocellular carcinoma (HCC) based on proliferative capacity, identify hub genes associated with highly proliferative HCC, and investigate its regulatory roles in HCC.
Materials and Methods: Bioinformatics analysis was employed to establish classification of HCC and further identify the hub gene. Cell counting kit-8 (CCK-8) assay, colony formation assay, Western Blot assay and tumor xenograft assay were employed to detect the proliferation of HCC cells. Transwell assay and Western blot assay were employed to detect the migration of HCC cells. RNA sequencing analysis was employed to explore the signaling pathways activated by the gene and verify it through rescue experiments.
Results: We classified HCC into three more precise subtypes termed Prolifer-low, Prolifer-mid and Prolifer-high, and also found that Cms1 ribosomal small subunit homolog 1 (CMSS1) was a hub gene associated with stronger proliferative capacity subgroup of HCC. Functional studies revealed that CMSS1 overexpression significantly promoted the proliferation of HCC cells in vitro and in vivo. Additionally, CMSS1 could also promote the migration and epithelial-mesenchymal transition of HCC cells. Mechanistically, RNA sequencing analysis revealed that CMSS1 knockdown inhibited the tumor necrosis factor (TNF) and downstream nuclear factor kappa B (NF-κB) signaling pathways. More importantly, TNF or NF-κB suppression could reverse the promoting effects of CMSS1 on HCC cells proliferation and migration.
Conclusion: The study suggested that CMSS1 could be a critical modulator of HCC tumorigenesis and metastasis through the TNF/NF-κB signaling pathway, thus being considered as a potential therapeutic target for HCC. Targeting CMSS1 may offer a novel strategy to inhibit NF-κB-driven inflammatory signaling and suppress tumor progression in HCC.
Keywords: CMSS1, HCC, proliferation, migration, TNF, NF-κB
1Department of Radiation and Medical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 430071, People’s Republic of China; 2Wuhan University Taikang Medical School (School of Basic Medical Sciences), Wuhan, Hubei, 430071, People’s Republic of China; 3Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, People’s Republic of China; 4Hubei Key Laboratory of Tumor Biological Behaviors, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 430071, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Jing Dai, Department of Radiation and Medical Oncology, Zhongnan Hospital of Wuhan University, 169 East Lake Road, Wuchang District, Wuhan, Hubei, 430071, People’s Republic of China, Email daijing@znhospital.cn Peng Zhang, Wuhan University Taikang Medical School (School of Basic Medical Sciences), 115 East Lake Road, Wuchang District, Wuhan, Hubei, 430071, People’s Republic of China, Email zhp@whu.edu.cn
Purpose: The study aims to further classify hepatocellular carcinoma (HCC) based on proliferative capacity, identify hub genes associated with highly proliferative HCC, and investigate its regulatory roles in HCC.
Materials and Methods: Bioinformatics analysis was employed to establish classification of HCC and further identify the hub gene. Cell counting kit-8 (CCK-8) assay, colony formation assay, Western Blot assay and tumor xenograft assay were employed to detect the proliferation of HCC cells. Transwell assay and Western blot assay were employed to detect the migration of HCC cells. RNA sequencing analysis was employed to explore the signaling pathways activated by the gene and verify it through rescue experiments.
Results: We classified HCC into three more precise subtypes termed Prolifer-low, Prolifer-mid and Prolifer-high, and also found that Cms1 ribosomal small subunit homolog 1 (CMSS1) was a hub gene associated with stronger proliferative capacity subgroup of HCC. Functional studies revealed that CMSS1 overexpression significantly promoted the proliferation of HCC cells in vitro and in vivo. Additionally, CMSS1 could also promote the migration and epithelial-mesenchymal transition of HCC cells. Mechanistically, RNA sequencing analysis revealed that CMSS1 knockdown inhibited the tumor necrosis factor (TNF) and downstream nuclear factor kappa B (NF-κB) signaling pathways. More importantly, TNF or NF-κB suppression could reverse the promoting effects of CMSS1 on HCC cells proliferation and migration.
Conclusion: The study suggested that CMSS1 could be a critical modulator of HCC tumorigenesis and metastasis through the TNF/NF-κB signaling pathway, thus being considered as a potential therapeutic target for HCC. Targeting CMSS1 may offer a novel strategy to inhibit NF-κB-driven inflammatory signaling and suppress tumor progression in HCC.
Keywords: CMSS1, HCC, proliferation, migration, TNF, NF-κB