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已发表论文
YK-4-279 通过调节 MAPK 级联反应诱导骨肉瘤细胞周期停滞、DNA 损伤反应和细胞凋亡
Authors Wang W, Zhang Y , Jia X , Han L, Xin M
Received 27 May 2025
Accepted for publication 22 December 2025
Published 26 December 2025 Volume 2025:19 Pages 11749—11766
DOI https://doi.org/10.2147/DDDT.S542983
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Leonidas Panos
Weifeng Wang,1– 3 Yuli Zhang,4,5 Xiuqin Jia,6 Liren Han,1 Ming Xin7
1Department of Orthopedic Surgery, Beijing Jishuitan Hospital Liaocheng Hospital, Liaocheng, Shandong, People’s Republic of China; 2Department of Orthopedic Surgery, Liaocheng People’s Hospital, Liaocheng, Shandong, People’s Republic of China; 3School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, People’s Republic of China; 4Department of Dermatology, Liaocheng People’s Hospital, Liaocheng, Shandong, People’s Republic of China; 5Department of Dermatology, The Second Hospital of Shandong University, Jinan, Shandong, People’s Republic of China; 6The Key Laboratory of Clinical Pharmacology, Liaocheng People’s Hospital, Liaocheng, Shandong, People’s Republic of China; 7The Key Laboratory of Molecular Pharmacology, Liaocheng People’s Hospital, Liaocheng, Shandong, People’s Republic of China
Correspondence: Ming Xin, The Key Laboratory of Molecular Pharmacology, Liaocheng People’s Hospital, Liaocheng, Shandong, People’s Republic of China, Email xinming137@163.com Liren Han, Department of Orthopedic Surgery, Beijing Jishuitan Hospital Liaocheng Hospital, Liaocheng, Shandong, People’s Republic of China, Email fuleco@126.com
Background: YK-4-279, a promising anticancer agent, has demonstrated therapeutic potential against various tumors. Osteosarcoma (OS), an aggressive bone cancer primarily affecting adolescents, lacks effective treatment options. Investigating YK-4-279’s mechanisms in OS is critical for evaluating its clinical utility.
Methods: Using in vitro models, we examined YK-4-279’s effects on OS cell viability, proliferation, apoptosis, cell cycle progression, and DNA damage. We also assessed its impact on MAPK signaling pathway activation. To clarify the pathway’s role, we combined YK-4-279 treatment with a P38 inhibitor.
Results: YK-4-279 markedly suppressed OS cell viability and proliferation, triggered G2/M phase arrest, and enhanced apoptosis and DNA damage. Furthermore, it activated the MAPK pathway, elevating phosphorylation of ERK1/2, JNK, and P38 MAPK. Co-treatment with a P38 inhibitor partially reversed these effects, confirming MAPK’s involvement in YK-4-279’s antitumor action.
Conclusion: YK-4-279 inhibits OS cell growth, induces DNA damage and cell cycle arrest, and promotes apoptosis via MAPK pathway activation. These findings highlight its strong therapeutic potential for OS treatment.
Keywords: YK-4-279, osteosarcoma, MAPK signaling pathway, cell cycle, DNA damage, apoptosis
1Department of Orthopedic Surgery, Beijing Jishuitan Hospital Liaocheng Hospital, Liaocheng, Shandong, People’s Republic of China; 2Department of Orthopedic Surgery, Liaocheng People’s Hospital, Liaocheng, Shandong, People’s Republic of China; 3School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, People’s Republic of China; 4Department of Dermatology, Liaocheng People’s Hospital, Liaocheng, Shandong, People’s Republic of China; 5Department of Dermatology, The Second Hospital of Shandong University, Jinan, Shandong, People’s Republic of China; 6The Key Laboratory of Clinical Pharmacology, Liaocheng People’s Hospital, Liaocheng, Shandong, People’s Republic of China; 7The Key Laboratory of Molecular Pharmacology, Liaocheng People’s Hospital, Liaocheng, Shandong, People’s Republic of China
Correspondence: Ming Xin, The Key Laboratory of Molecular Pharmacology, Liaocheng People’s Hospital, Liaocheng, Shandong, People’s Republic of China, Email xinming137@163.com Liren Han, Department of Orthopedic Surgery, Beijing Jishuitan Hospital Liaocheng Hospital, Liaocheng, Shandong, People’s Republic of China, Email fuleco@126.com
Background: YK-4-279, a promising anticancer agent, has demonstrated therapeutic potential against various tumors. Osteosarcoma (OS), an aggressive bone cancer primarily affecting adolescents, lacks effective treatment options. Investigating YK-4-279’s mechanisms in OS is critical for evaluating its clinical utility.
Methods: Using in vitro models, we examined YK-4-279’s effects on OS cell viability, proliferation, apoptosis, cell cycle progression, and DNA damage. We also assessed its impact on MAPK signaling pathway activation. To clarify the pathway’s role, we combined YK-4-279 treatment with a P38 inhibitor.
Results: YK-4-279 markedly suppressed OS cell viability and proliferation, triggered G2/M phase arrest, and enhanced apoptosis and DNA damage. Furthermore, it activated the MAPK pathway, elevating phosphorylation of ERK1/2, JNK, and P38 MAPK. Co-treatment with a P38 inhibitor partially reversed these effects, confirming MAPK’s involvement in YK-4-279’s antitumor action.
Conclusion: YK-4-279 inhibits OS cell growth, induces DNA damage and cell cycle arrest, and promotes apoptosis via MAPK pathway activation. These findings highlight its strong therapeutic potential for OS treatment.
Keywords: YK-4-279, osteosarcoma, MAPK signaling pathway, cell cycle, DNA damage, apoptosis