Fig 2: MTE inhibited tumor angiogenesis in the HCC-PDX mouse model. (A) Representative images of IHC of angiogenesis-associated proteins (CD31, PDGFRB, VWF, PDGFB, and VEGF) on pathological slides of HCC-PDX tissues from control, MTE-L, MTE-M, and MTE-H groups. (B) Score of CD31, PDGFB, VEGF, PDGFRB, and VWF positive staining in these slides. Magnification: ×200. Compared with control, *p < 0.05; **p < 0.01; ***p < 0.001. Compared with MTE-L, # p < 0.05; ## p < 0.01; ### p < 0.001.

Fig 3: Identification and verification of differentially expressed genes (DEGs) between HCC cells treated with or without MTE. (A) HepG2 cells were treated with vehicle, 1.5 mg/ml MTE, or 3.0 mg/ml MTE for 24 h and subjected to RNA-sequencing. The clustering of differentially expressed genes of control vs. MTE-1.5 mg/ml and control vs. MTE-3.0 mg/ml was presented. The DEGs associated with metabolism and angiogenesis were clustered. (B) mRNA expression levels of VWF, VEGFR, and PDGFRB in MHCC97H and HepG2 cells treated with or without MTE. (C) Protein levels of VWF, VEGFR, and PDGFRB in HCC cells treated with or without MTE. *p < 0.05; **p < 0.01.

Fig 4: Experimental design. (A) A single fraction of 15 Gy/30 Gy with 6-MeV electrons is delivered to the dorsal skin using a linear accelerator. All parts of the body, except the irradiation field (back skin 2 × 2 cm), are protected with a lead plate, and a 1.0-cm tissue equivalent material is placed. (B) Representative photograph of the skin damage 20 days after radiation exposure. (C) RTOG score of radiation-induced dermatitis in the dorsal skin of two different groups of mice (adapted from 72 ); n = 4–5 mice per group. (D) Immunofluorescence staining of Pdgfrb and Atg7 in the control group (Atg7F/F Cre-) mice and myofibroblast-specific conditional Atg7 knockout (Atg7F/F Cre+) mice. Scale bar: 50 µm. Statistical significance was estimated using the Mann–Whitney U test; *p < 0.05, Z = -2.425.