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Fig. 2 | Journal of Translational Medicine

Fig. 2

From: LIPH contributes to glycolytic phenotype in pancreatic ductal adenocarcinoma by activating LPA/LPAR axis and maintaining ALDOA stability

Fig. 2

LIPH promoted proliferation and inhibited apoptosis of pancreatic cancer cells in vitro. A LIPH expression in pancreatic cancer cell lines (MIA PaCa-2, HPNE, 8988s, 8988t, PANC-1, BxPC-3, AsPC-1 and CFPAC-1) compared with that in normal pancreatic ductal epithelial cell line HPNE, detected by qPCR and Western Blotting. B The mRNA and protein expression of LIPH in LIPH-knockdown PANC-1 and CFPAC-1 cells. C The colony formation ability was inhibited by LIPH knockdown. D The CCK8 assay showed that LIPH knockdown in PANC-1 and CFPAC-1 resulted in suppression of proliferation ability. E Flow cytometric apoptosis assay and BAX protein expression (starvation) were used to detect the apoptosis level following LIPH knockdown (−FBS: Medium without FBS; + GEM: Medium with Gemcitabine). F After 72 h serum deprivation, the CCK8 assays were used to detect cell proliferation ability. For positive control, 10% FBS was used to culture cancer cells. G CFPAC-1 and PANC-1 cells were cultured one day in 0.5% FAF-BSA complete medium (starvation), and then exogenous PA (10 µM) or LPA (10 µM) were added to the cultured cells, followed by CCK8 assays at 72 h to detect cell proliferation ability. *P < 0.05, **P < 0.01, ***P < 0.001 and ****P < 0.0001

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