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Fig. 6. Role of <t>XIAP</t> in limocitrin -induced apoptosis activation. (A) Reduced XIAP expression observed in SCC-9 and SCC-47 cells after 24 h of limocitrin treatment. (B) Quantitative analysis of <t>XIAP,</t> <t>cIAP-1,</t> p-HSP27 and HSP27 levels in SCC-9 and SCC-47 cell lines. (C, F) Cotreatment of SCC-9 with siRNA negative control (si-NC), XIAP siRNA (si-XIAP), and limocitrin. Quantitation of cleaved PARP, caspase-3, and caspase-8 is illustrated. (D, G) Cotreatment of SCC-9 with cIAP-1 siRNA (si-cIAP1) and limocitrin. Quantitation of cleaved PARP, caspase-3, and caspase-8 is illustrated. (E, H) Cotreatment of SCC-9 with HSP27 siRNA (si- HSP27) and limocitrin. Quantitation of cleaved PARP, caspase-3, and caspase-8 is illustrated. All data are displayed as mean ± standard deviation (n = 3). *p < 0.05, indicating statistical significance compared with the control group. #p < 0.05, indicating statistical significance compared with limocitrin treatment alone.
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Fig. 6. Role of <t>XIAP</t> in limocitrin -induced apoptosis activation. (A) Reduced XIAP expression observed in SCC-9 and SCC-47 cells after 24 h of limocitrin treatment. (B) Quantitative analysis of <t>XIAP,</t> <t>cIAP-1,</t> p-HSP27 and HSP27 levels in SCC-9 and SCC-47 cell lines. (C, F) Cotreatment of SCC-9 with siRNA negative control (si-NC), XIAP siRNA (si-XIAP), and limocitrin. Quantitation of cleaved PARP, caspase-3, and caspase-8 is illustrated. (D, G) Cotreatment of SCC-9 with cIAP-1 siRNA (si-cIAP1) and limocitrin. Quantitation of cleaved PARP, caspase-3, and caspase-8 is illustrated. (E, H) Cotreatment of SCC-9 with HSP27 siRNA (si- HSP27) and limocitrin. Quantitation of cleaved PARP, caspase-3, and caspase-8 is illustrated. All data are displayed as mean ± standard deviation (n = 3). *p < 0.05, indicating statistical significance compared with the control group. #p < 0.05, indicating statistical significance compared with limocitrin treatment alone.
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Fig. 6. Role of <t>XIAP</t> in limocitrin -induced apoptosis activation. (A) Reduced XIAP expression observed in SCC-9 and SCC-47 cells after 24 h of limocitrin treatment. (B) Quantitative analysis of <t>XIAP,</t> <t>cIAP-1,</t> p-HSP27 and HSP27 levels in SCC-9 and SCC-47 cell lines. (C, F) Cotreatment of SCC-9 with siRNA negative control (si-NC), XIAP siRNA (si-XIAP), and limocitrin. Quantitation of cleaved PARP, caspase-3, and caspase-8 is illustrated. (D, G) Cotreatment of SCC-9 with cIAP-1 siRNA (si-cIAP1) and limocitrin. Quantitation of cleaved PARP, caspase-3, and caspase-8 is illustrated. (E, H) Cotreatment of SCC-9 with HSP27 siRNA (si- HSP27) and limocitrin. Quantitation of cleaved PARP, caspase-3, and caspase-8 is illustrated. All data are displayed as mean ± standard deviation (n = 3). *p < 0.05, indicating statistical significance compared with the control group. #p < 0.05, indicating statistical significance compared with limocitrin treatment alone.
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Fig. 6. Role of <t>XIAP</t> in limocitrin -induced apoptosis activation. (A) Reduced XIAP expression observed in SCC-9 and SCC-47 cells after 24 h of limocitrin treatment. (B) Quantitative analysis of <t>XIAP,</t> <t>cIAP-1,</t> p-HSP27 and HSP27 levels in SCC-9 and SCC-47 cell lines. (C, F) Cotreatment of SCC-9 with siRNA negative control (si-NC), XIAP siRNA (si-XIAP), and limocitrin. Quantitation of cleaved PARP, caspase-3, and caspase-8 is illustrated. (D, G) Cotreatment of SCC-9 with cIAP-1 siRNA (si-cIAP1) and limocitrin. Quantitation of cleaved PARP, caspase-3, and caspase-8 is illustrated. (E, H) Cotreatment of SCC-9 with HSP27 siRNA (si- HSP27) and limocitrin. Quantitation of cleaved PARP, caspase-3, and caspase-8 is illustrated. All data are displayed as mean ± standard deviation (n = 3). *p < 0.05, indicating statistical significance compared with the control group. #p < 0.05, indicating statistical significance compared with limocitrin treatment alone.
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Fig. 6. Role of XIAP in limocitrin -induced apoptosis activation. (A) Reduced XIAP expression observed in SCC-9 and SCC-47 cells after 24 h of limocitrin treatment. (B) Quantitative analysis of XIAP, cIAP-1, p-HSP27 and HSP27 levels in SCC-9 and SCC-47 cell lines. (C, F) Cotreatment of SCC-9 with siRNA negative control (si-NC), XIAP siRNA (si-XIAP), and limocitrin. Quantitation of cleaved PARP, caspase-3, and caspase-8 is illustrated. (D, G) Cotreatment of SCC-9 with cIAP-1 siRNA (si-cIAP1) and limocitrin. Quantitation of cleaved PARP, caspase-3, and caspase-8 is illustrated. (E, H) Cotreatment of SCC-9 with HSP27 siRNA (si- HSP27) and limocitrin. Quantitation of cleaved PARP, caspase-3, and caspase-8 is illustrated. All data are displayed as mean ± standard deviation (n = 3). *p < 0.05, indicating statistical significance compared with the control group. #p < 0.05, indicating statistical significance compared with limocitrin treatment alone.

Journal: Scientific reports

Article Title: Limocitrin induced cellular death through ERK pathways in human oral squamous cell cancer.

doi: 10.1038/s41598-025-02178-6

Figure Lengend Snippet: Fig. 6. Role of XIAP in limocitrin -induced apoptosis activation. (A) Reduced XIAP expression observed in SCC-9 and SCC-47 cells after 24 h of limocitrin treatment. (B) Quantitative analysis of XIAP, cIAP-1, p-HSP27 and HSP27 levels in SCC-9 and SCC-47 cell lines. (C, F) Cotreatment of SCC-9 with siRNA negative control (si-NC), XIAP siRNA (si-XIAP), and limocitrin. Quantitation of cleaved PARP, caspase-3, and caspase-8 is illustrated. (D, G) Cotreatment of SCC-9 with cIAP-1 siRNA (si-cIAP1) and limocitrin. Quantitation of cleaved PARP, caspase-3, and caspase-8 is illustrated. (E, H) Cotreatment of SCC-9 with HSP27 siRNA (si- HSP27) and limocitrin. Quantitation of cleaved PARP, caspase-3, and caspase-8 is illustrated. All data are displayed as mean ± standard deviation (n = 3). *p < 0.05, indicating statistical significance compared with the control group. #p < 0.05, indicating statistical significance compared with limocitrin treatment alone.

Article Snippet: The primary antibodies against cyclin E1 #20,808, cyclin E2 #4132, p21 #2947, CDK2 #2546, CDK4 #12,790, CDK6 #3136, Fas #4233, DR5 #8074, DcR3 #4758, DcR2 #8049, Bax #5023, Bak #3814, Bcl-2 #3498, Bcl-xL #2764, c-caspase 3 #9664, c-caspase 8 #9496, c-caspase 9 #9502, c-PARP #5625, p-AKT #4060, AKT #2920, p-ERK #4370, ERK #4695, p38 #9212, p-JNK #4668, JNK #9258, XIAP #14,334, cIAP-1 #7065, HSP-27 #95,357, p-HSP-27 #9709 and β-actin #4970 were purchased from Cell Signaling Technology, Danvers, MA, USA; antibody against p-p38 #44-684G was purchased from Invitrogen, Carlsbad, MA, USA.

Techniques: Activation Assay, Expressing, Negative Control, Quantitation Assay, Standard Deviation, Control