Skip to main content
Fig. 6 | Military Medical Research

Fig. 6

From: Elevated FBXL6 activates both wild-type KRAS and mutant KRASG12D and drives HCC tumorigenesis via the ERK/mTOR/PRELID2/ROS axis in mice

Fig. 6

Elevated PRELID2 is positively correlated with the FBXL6/p-ERK/p-mTOR pathway and poor prognosis of HCC. a Representative images of IHC staining for FBXL6, PRELID2, p-ERK, and p-mTOR in human HCC tumors. Scale bar = 50 µm. b The association between PRELID2 and FBXL6, p-ERK, or p-mTOR in 129 paired HCC tumors and adjacent normal tissues was analyzed by χ2 test. c The prognostic significance of PRELID2 in HCC patients was evaluated by Kaplan–Meier analysis. High expression of PRELID2 predicted a shorter overall survival (OS) time. d The association between FBXL6 and p-ERK/p-mTOR protein levels in 129 HCC tissues was evaluated by the χ2 test. e The prognostic significance of the coexpression of FBXL6 and p-ERK in HCC patients was evaluated by Kaplan–Meier analysis. f Kaplan–Meier survival curves showing the overall survival of FBXL6high/p-ERKhigh HCC patients with high or low PRELID2 expression. PRELID2 the proteins of relevant evolutionary and lymphoid interest (PRELI) domain 2, FBXL6 F-box and leucine-rich repeat 6, ERK extracellular signal-regulated kinase, mTOR mammalian target of rapamycin, IHC immunohistochemistry, HCC hepatocellular carcinoma

Back to article page