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Fig. 3 | BMC Cancer

Fig. 3

From: A novel treatment strategy for lapatinib resistance in a subset of HER2-amplified gastric cancer

Fig. 3

Protein interaction network prediction, gene expression profile and pathway analysis of CSK or PTEN knockout cell lines and Up-regulation of PI3K/AKT and MAPK pathways in the CSK or PTEN knockout GC cells. Protein interaction network (a) and the predicted partners (b) were analyzed by STRING. CSK, PTEN and HER2 (ERBB2) were mapped by searching the STRING database version 10.5. In the resulting protein association network, proteins are presented as nodes which are connected by lines whose thickness represents the confidence level. (c) The bar plot depicts the enriched pathway among the DEGs between CSK null cells (N87-CSK-sgRNA) and parental N87 cells (N87) by KEGG pathway analysis. d The bar plot depicts the enriched pathway among the DEGs between PTEN null cells (OE19-PTEN-sgRNA) and parental OE19 cells (OE19) by KEGG pathway analysis. e The levels of phosphorylated and total proteins of AKT and MAPK were assessed by western blotting in CSK or PTEN knockout OE19 cells after treating with 0.05 uM lapatinib, respectively. OE19 cells transduced with non-targeting sgRNA as control. f The levels of phosphorylated and total proteins of AKT and MAPK were assessed by western blots in CSK or PTEN knockout N87 cells after treating with 0.01 um lapatinib, respectively. N87 cells transduced with non-targeting sgRNA as control. g PTEN and CSK protein expression was examined by western blotting in CSK knockout OE19 cell lines and PTEN knockout OE19 cell lines, respectively. OE19 cells transduced with non-targeting sgRNA as control. h PTEN protein and CSK protein expression was examined by western blotting in CSK knockout N87 cell lines and PTEN knockout N87 cell lines, respectively. N87 cells transduced with non-targeting sgRNA as control

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