Additional file 1 of Exosomal lncRNA TUG1 from cancer-associated fibroblasts promotes liver cancer cell migration, invasion, and glycolysis by regulating the miR-524-5p/SIX1 axis

Additional file 1. Table S1. Clinicopathological characteristics and follow-up data of 120 patients with HCC. Table S2. Primes sequences used in this study. Figure S1. Characterization of CAFs and NFs. Microscopic observation of primary CAFs and NFs. Scale bar: 100 m.Figure S2. Identification and internalization of exosomes. (A) TEM images of CAFs/NFs-derived exosomes (CAFs-exo/NFs-exo) (scale bar: 200 nm). (B) Protein levels of exosomal markers CD63, CD9, and TSG101. (C) Confocal microscopic images showing internalization of exosomes by HepG2 cells (scale bar: 50 m).Figure S3. Effects of CAFs-derived exosomal TUG1 on HepG2 cell metastasis in vivo. Effects of exosomes derived from the CAFs with or without TUG1 shRNA adenovirus infection on (A, B) metastasis (scale bar: 200 m) (n = 6) and (C) survival duration of mice (n = 15). The data are expressed as the mean + SD (n = 6). ***P < 0.001 vs blank. ###P < 0.001 vs CAFs-exo.Figure S4. The effects of CAFs-derived exosomes on HepG2 cells are inhibited by TUG1 knockdown. (A, B) Migration and invasion, (C) glucose uptake, (D) LDH activity, (E) lactate, and (F) ATP content, (G) TUG1 expression, and (H, I) MMP-2, MMP-9, HK2, and LDHA expressions were measured in HepG2 treated with CAFs-exo and transduced with shTUG1 or shNC. The data are expressed as the mean + SD (n = 3). ***P < 0.001 compared with shNC.