Fig. 7

LncRNA PART1 mediates Bcl-2 expression through functioning as a ceRNA for miR-129. a Presentation of score of lncRNA PART1 at different subcellular locations by lncLocator (http://www.csbio.sjtu.edu.cn/bioinf/lncLocator/). b The expression level of PART1 in nuclear and cytoplasm of ESCC cells. U1 (nuclear retained) and GAPDH (exported to cytoplasm) were used as controls. c FISH analysis of the subcellular location of PART1 with specific probe in ESCC cells. d RIP experiments were performed using the AGO2 antibody, and specific primers were used to detect the enrichment of PART1 and Bcl-2 in TE1/GR cells. e RIP assay of the enrichment of Ago2 on lncRNA PART1 and Bcl-2 transcripts relative to IgG in ESCC cells transfected with pcDNA-PART1. ^**P < 0.01, ^***P < 0.001 compared to p-vector group. f Representation of the miR-129 binding sites in lncRNA PART1 based on miRcode (http://www.mircode.org/mircode/), and Bcl-2 binding sites in miR129 on TargetScan (http://www.targetscan.org/). g RT-qPCR analysis of miR-129 expression in gefitinib resistant and sensitive cells. ^*P < 0.05 compared to parental cell group. h Verification of Bcl-2 level after transfection with miR-129 mimics at transcript (upper panel) and protein (lower panel) level. ^**P < 0.01 compared to NC mimics group i-k Firefly luciferase activity normalized to Renilla luciferase activity (FURL ratio) in ESCC cells co-transfected with luciferase reporters with wild type transcripts of PART1 (i), Bcl-2 (j), and mutant type transcript Bcl-2 (k) along with miR-129 mimics or negative control (NC mimics). ^*P < 0.05, ^**P < 0.01 compared to NC mimics group. l-m RIP experiments were performed in cells overexpressed (l) or downregulated (m) PART1 using a Bcl-2 antibody to immunoprecipitate RNA and a primer to detect miR-129. ^*P < 0.05 compared to Bcl-2 antibody (negative control/vector) group