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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: LncRNA CBR3-AS1 regulates of breast cancer drug sensitivity as a competing endogenous RNA through the JNK1/MEK4-mediated MAPK signal pathway

Fig. 1

CBR3-AS1 expression is up-regulated in breast cancer-resistant cells and is related to drug sensitivity and poor prognosis of breast cancer. a, b Gene chip analysis of lncRNA transcripts in MCF-7/ADR cells and MCF-7 cells. c The top 20 lncRNAs with the most obvious up-regulation and downregulation in MCF-7/ADR cells. d qRT-PCR analysis of the expression of five lncRNAs in MCF-7/ADR cells and MCF-7 cells. e The correlation between CBR3-AS1 expression and the IC50 value of ADR in 44 breast cancer cell lines in the CCLE and GDSC databases. f The IC50 value of ADR was detected for both sensitive and resistant cells by the CCK-8 assay. g CBR3-AS1 expression in four breast cancer cell lines. h Expression of CBR3-AS1 in normal tissues and breast cancer tissues from the TCGA database. i GSEA analysis of CBR3-AS1 enrichment in the ABC transporter signaling pathway. j, k Correlation analysis between CBR3-AS1 and both P-gp mRNA and BCRP mRNA from the TGCA database. l Kaplan-Meier survival analysis based on CBR3-AS1 expression in breast cancer patients (p = 0.0482). m CBR3-AS1 expression in breast cancer patients as determined by ISH. Original magnification, × 200. Scale bars, 100 μm. n Kaplan-Meier survival analysis of breast cancer patients based on CBR3-AS1 expression in our cohort (n = 96, p = 0.044). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001

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