Fig 2: Distant metastasis-free survival of ER+ breast cancer patients, stratified by ANGPT2 expression. Kaplan–Meier analysis comparing distant metastasis-free survival of ER+ breast cancer patients following endocrine therapy (n = 561, A) and those without endocrine therapy (n = 435, B), distinguished by low versus high expressions of ANGPT2. Gene expression data obtained from the open-source KM Plotter (Szasz et al. 2016). Beeswarm graph plots of each RNA prove distribution. ANGPT2, angiopoietin-2 mRNA; ER, estrogen receptor.

Fig 3: Immunohistochemistry analysis of BMAL1, HIF-1a, ANG1, ANG2, and VEGF expression in glioma and normal tissues with different pathological grades.

Fig 4: High expression of Ang2 in lung cancer tissue and serum samples. (A) Human lung cancer and normal lung tissue samples and lung cancer cell line A549 were used to purify proteins, and Ang2 expression was measured by Western blot. (B) Blood serum samples were collected from patients and controls and analyzed by enzyme-linked immunosorbent assay (ELISA). The results are expressed as the mean ± standard error of the mean (S.E.M.) of three separate experiments.

Fig 5: The PRMT5/MEP50/WDR5 is involved in MYBL1-induced angiogenesis via epigenetically regulation of ANGPT2.A Schematic of dCas9-mediated capture of chromatin interactions between MYBL1 and PRMT5. B Co-IP assay showing that endogenous MYBL1 interacted with endogenous PRMT5 in HCC cells. C Heatmap of ChIP-qPCR enrichments of histone post-translational modifications on MYBL1 promoter in the indicated cells. D ChIP-qPCR enrichments of H3R2me1 and H3R2me2s on ANGPT2 promoter region in the indicated group. E ChIP-qPCR enrichments of H3K4me3, polymerase II, or IgG on ANGPT2 promoter region in the indicated group. F Quantification of HUVEC tube formation cultured on Matrigel-coated plates in the indicated group. G Cell migration assay was performed by culturing HUVEC with conditioned media in the indicated group.