Current pharmaceutical design · 2026
Kunxian Capsule Exerts Antitumor Effects by Activating the IL-17 Signaling Pathway to Inhibit the Proliferation, Apoptosis, Cell Cycle, and Induce Reactive Oxygen Species Production in C8166 Tumor Cells.
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Wang Xiao-Dan, Ma Xiao-Na, Fang Chun-Sheng, Qin Ren-An, He Feng-Lei, Lin Yun-Bin, Xu Qiang, Li Nan
Аннотация
INTRODUCTION: Kunxian capsule (KXJN), a patented traditional Chinese medicine used for autoimmune diseases, remains unexplored in oncology. This study investigated its potential antitumor effects against adult T-cell leukemia/lymphoma (A-ATL).
METHODS: Network pharmacology identified KXJN-related targets from TCMSP and UniProt, and A-ATLassociated DEGs from GEO. Candidate targets and pathways were analyzed via Microbiotics and String. In vitro validation used C8166 cells, assessing proliferation (MTT assay), apoptosis, cell cycle, ROS production (flow cytometry), and protein/mRNA expression (Western blot, RT-qPCR).
RESULTS: A total of 106 potential targets of KXJN were identified against A-ATL, with core nodes (JUN, IL-6, TNF) linked to the IL-17 pathway and other pathways. KXJN dose- and time-dependently inhibited C8166 proliferation, promoted apoptosis, and increased ROS. It activated the IL-17 pathway, upregulating associated proteins (ACT1, IL-17RA, TRAF6), core targets (JUN, IL-6, TNF), and cytokines (CXCL1, CXCL2, CCL20).
DISCUSSION: KXJN exerts antitumor effects on C8166 cells by suppressing proliferation, inducing apoptosis and ROS, activating IL-17 signaling, and modulating cell cycle progression.
CONCLUSION: These findings highlight KXJN's potential in tumor therapy, though further in vitro and in vivo studies are required to elucidate its precise mechanisms.
METHODS: Network pharmacology identified KXJN-related targets from TCMSP and UniProt, and A-ATLassociated DEGs from GEO. Candidate targets and pathways were analyzed via Microbiotics and String. In vitro validation used C8166 cells, assessing proliferation (MTT assay), apoptosis, cell cycle, ROS production (flow cytometry), and protein/mRNA expression (Western blot, RT-qPCR).
RESULTS: A total of 106 potential targets of KXJN were identified against A-ATL, with core nodes (JUN, IL-6, TNF) linked to the IL-17 pathway and other pathways. KXJN dose- and time-dependently inhibited C8166 proliferation, promoted apoptosis, and increased ROS. It activated the IL-17 pathway, upregulating associated proteins (ACT1, IL-17RA, TRAF6), core targets (JUN, IL-6, TNF), and cytokines (CXCL1, CXCL2, CCL20).
DISCUSSION: KXJN exerts antitumor effects on C8166 cells by suppressing proliferation, inducing apoptosis and ROS, activating IL-17 signaling, and modulating cell cycle progression.
CONCLUSION: These findings highlight KXJN's potential in tumor therapy, though further in vitro and in vivo studies are required to elucidate its precise mechanisms.