Fig. 2: Supermeres exhibit a distinct proteome with high levels of TGFBI.
a, Venn diagram of unique and common proteins identified in DiFi-derived sEVs, NV fractions, exomeres and supermeres. b, Principal component (PC) analysis of normalized DiFi proteomic mass spectral counts. c, Heatmap of the top-20 most abundant proteins in each of the samples from DiFi cells. d, Venn diagram of unique and common top-50 most abundant proteins identified in supermeres derived from DiFi, PANC-1 and MDA-MB-231 cells. e, Immunoblot of representative proteins in DiFi- (top), PANC-1- (middle) and MDA-MB-231-derived (bottom) supermeres. Equal quantities (30 µg) of protein from each fraction were analysed. f, FAVS analysis of the TGFBI levels in the sEV-P (left), exomeres (middle) and supermeres (right) derived from DiFi cells. g, Immunohistochemical staining of TGFBI expression in normal (NL) colon and CRC tissue samples. Data are representative of three independent experiments. Scale bars, 100 µm. h,i, Overall (h) and progression-free (i) survival analysis of patients with CRC with different levels of TGFBI (that is, high versus low) using the Kaplan–Meier method; data were compared between the two marker groups using a two-sided log-rank test. j, ELISA analysis of the TGFBI levels in supermeres derived from plasma from control individuals (NL1–3) and patients with CRC. Data are the mean of n = 3 technical replicates. k, FAVS analysis of the TGFBI levels in sEV-Ps, exomeres and supermeres derived from the plasma of patients with CRC. f,k, The red boxes indicate TGFBI-positive particles. The percentages indicate the percent of particles that contain TGFBI above the detection limit. WCL, whole-cell lysate; exom, exomere; and super, supermere.
