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. 2022 Feb 22;27:17. doi: 10.1186/s11658-022-00309-9

Fig. 3.

Fig. 3

CAFs-derived exosomal TUG1 promotes migration, invasion, and glycolysis in HepG2 cells. A Expression levels of TUG1, GAS5, H19, MALAT1, MEG3, NEAT1, and XIST in NFs-exo and CAFs-exo as measured by qPCR. B TUG1 level in HepG2 treated with NFs-exo or CAFs-exo determined by qPCR. C TUG1 level in exosomes derived from the CAFs transduced with TUG1 shRNA or shNC determined by qPCR assay. Effects of exosomes derived from CAFs transduced with TUG1 shRNA or shNC, and TUG1 overexpression in HepG2 cells on (D, E) migration and invasion, (F) glucose uptake, (G) LDH activity, (H) lactate, and (I) ATP content, (J) TUG1 expression, and (K, L) MMP-2, MMP-9, HK2, and LDHA. The data are expressed as the mean ± SD (n = 3). **P < 0.01, ***P < 0.001 vs NFs-exo, blank (HepG2 cells without treatment), shNC or CAFs/shNC-exo. ###P < 0.001 vs corresponding CAFs/shTUG1-exo + Vector