MOESM3 of Simultaneously inactivating Src and AKT by saracatinib/capivasertib co-delivery nanoparticles to improve the efficacy of anti-Src therapy in head and neck squamous cell carcinoma

Additional file 3: Figure S3. The effect of indicated treatment on other Src-related proteins (including STAT3, FAK and EGFR) in HNSCC cells

MOESM2 of Simultaneously inactivating Src and AKT by saracatinib/capivasertib co-delivery nanoparticles to improve the efficacy of anti-Src therapy in head and neck squamous cell carcinoma

Additional file 2: Figure S2. The effect of indicated treatment on cell viability determined by CellTiter-Glo® Luminescent Cell Viability Kit at 72 hours after treatment. ns: not significant; *p<0.05; **p<0.01

MOESM4 of Simultaneously inactivating Src and AKT by saracatinib/capivasertib co-delivery nanoparticles to improve the efficacy of anti-Src therapy in head and neck squamous cell carcinoma

Additional file 4: Figure S4. The average weight of tongue and body in HN8- (A) and HN12-derived orthotopic xenograft mice (B) during different treatments. *p<0.05; **p<0.01

MOESM1 of Simultaneously inactivating Src and AKT by saracatinib/capivasertib co-delivery nanoparticles to improve the efficacy of anti-Src therapy in head and neck squamous cell carcinoma

Additional file 1: Figure S1. Constitutive activation of AKT signaling enhances the resistance of saracatinib in HN8 cells. (A) The effect of AKT-CA transfection on AKT activation determined by Western blotting. (B) The effect of AKT-CA transfection on cell viability in the presence or absence of saracatinib determined by CellTiter-Glo® Luminescent Cell Viability Kit on day 3 after treatment. *p<0.05; **p<0.01

MOESM6 of Simultaneously inactivating Src and AKT by saracatinib/capivasertib co-delivery nanoparticles to improve the efficacy of anti-Src therapy in head and neck squamous cell carcinoma

Additional file 6: Figure S6. The levels of phospho-Src and Ki67 in HN8-derived orthotopic xenograft tumors receiving different treatments determined by IHC. The representative IHC images were shown in (A) and quantification of IHC staining using Image pro-Plus6.0 was shown in (B). *p<0.05; **p<0.01

MOESM5 of Simultaneously inactivating Src and AKT by saracatinib/capivasertib co-delivery nanoparticles to improve the efficacy of anti-Src therapy in head and neck squamous cell carcinoma

Additional file 5: Figure S5. Histology examination of tissues taken from mouse major organs (heart, intestine, kidney, liver, lung and spleen) at the endpoint of each indicated treatment

Additional file 5: Figure S5. of FGF19/FGFR4 signaling contributes to the resistance of hepatocellular carcinoma to sorafenib

FGF19 knockdown in sorafenib-resistant HepG2 cells enhances ROS-associated apoptosis by sorafenib. (A) The knockdown effect of FGF19 in Sora-resistant HepG2 (HepG2 Sora-R) cells. (B–E) The effect of FGF19 knockdown on Sora-induced apoptosis in HepG2 Sora-R cells. FGF19 was knocked down in HepG2 Sora-R cells by lentiviral shRNA. FGF19 knockdown cells (shFGF19) and the control cells (shNC) were treated with different doses of Sora for 24 h. Cell viability was determined by MTS assays (B); apoptosis was determined by DAPI staining (C); ROS generation was determined by DCFH-DA staining (D), and O2 •− generation was determined by electrochemical biosensor (E). In A, expression levels were normalized against actin and reported relative to controls (fold changes shown below each lane). * p < 0.05; ** p < 0.01

MOESM7 of Simultaneously inactivating Src and AKT by saracatinib/capivasertib co-delivery nanoparticles to improve the efficacy of anti-Src therapy in head and neck squamous cell carcinoma

Additional file 7: Figure S7. Blood biochemical indexes of NSG mice following intravenous administration of indicated treatment. In this study, AST (A) and ALT (B) levels reflect hepatic functions, and creatinine (C) levels reflect nephron functions. *p < 0.05; **p < 0.01

Additional file 5: of Combating head and neck cancer metastases by targeting Src using multifunctional nanoparticle-based saracatinib

Figure S5. Mice were sacrificed on day 12 after treatment, and xenografts were dissected and removed for Western blot with the indicated antibodies. The representative image of Western blot was shown in the left panel, and quantitative data of p-Src levels were shown in the right panel (n = 5). 1, 2, and 3 indicate the tumor samples from three different mice. **p < 0.01. (DOCX 40 kb

Additional file 2: of Combating head and neck cancer metastases by targeting Src using multifunctional nanoparticle-based saracatinib

Figure S2. MTS analysis of HN12 cell proliferation in the treatment of saracatinib and Nano-sar within 96 h. (DOCX 23 kb