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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: Exosome-mediated transfer of lncRNA PART1 induces gefitinib resistance in esophageal squamous cell carcinoma via functioning as a competing endogenous RNA

Fig. 2

LncRNA PART1 is activated by transcription factor STAT1. a STAT1 binding site prediction in the PART1 promoter region using JASPAR. b The expression of STAT1 in gefitinib resistant and normal cells at transcript (left panel) and protein (right panel) levels. *P < 0.05 compared to ESCC parental cell group. c RT-qPCR verification of the upregulation of STAT1 after transfection of specific plasmid vectors. ***P < 0.001 compared to pcDNA-vector group. d RT-qPCR analysis of lncRNA PART1 expression after STAT1 was overexpressed. *P < 0.05 compared to p-vector group. e FISH analysis of the enriched level of STAT1 gene in nucleus of TE1 or TE1/GR cells. ***P < 0.001 compared to TE1 cells. f ChIP assay was performed to detect the relative enrichment of STAT1 on promoter region of lncRNA PART1. *P < 0.05, **P < 0.01, ***P < 0.001 compared to TE1 cell group. g Schematic presentation STAT1 binding sites in the promoter region of PART1. h Luciferase activity analysis of the three binding sites in cells transfected with respective oligonucleotides. *P < 0.05 compared to p-vector group

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