Fig. 6

GNAS promotes LPS-induced STAT3 activation in HCC cells through inhibiting long non-coding RNA TPTEP1 interacting with STAT3. a HepG2 cells or GNAS knockout-HepG2 cells were treated with LPS (5 μg/ml) or not for the indicated hours. Then, the interactions of JAK1/2, STAT3 and GNAS were detected by CO-IP. b HepG2 cells were treated with LPS (5 μg/ml) or MED for 12 h, and then the protein expression levels of STAT3 and GNAS in the cytoplasmic and nuclear fractions were detected by Western blotting (GAPDH as the cytoplasmic marker, and histone H3 as the nuclear marker). c HepG2 cells or GNAS knockout-HepG2 cells were treated with LPS (5 μg/ml) or not for 12 h. The interaction between STAT3 and TPTEP1 was detected by RIP. d HepG2 cells were transfected with pCMV-myc vector or pCMV-myc-GNAS for 24 h, and then treated with LPS (5 μg/ml) or not for 12 h. The interaction between STAT3 and TPTEP1 was detected by RIP. e The interaction between biotin-labeled TPTEP1 and STAT3 in HepG2 cells or GNAS knockout HepG2 cells was detected by RNA pull-down. f The interaction between biotin-labeled TPTEP1 and STAT3 in HepG2 cells or GNAS overexpressed-HepG2 cells was detected by RNA pull-down. Data are represented as means ± SD (n = 3; ^*represents P < 0.05)