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Fig. 5 | Journal of Translational Medicine

Fig. 5

From: HDAC inhibitor ITF2357 reduces resistance of mutant-KRAS non-small cell lung cancer to pemetrexed through a HDAC2/miR-130a-3p-dependent mechanism

Fig. 5

HDAC inhibitor ITF2357 reduces the resistance of mut-KRAS NSCLC cells to Pem by inhibiting HDAC2/miR-130a-3p. A Heatmap of differentially expressed genes between control samples and NSCLC samples in GSE102286 (normal = 88, tumor = 91). B Venn map shows the overlap of the downregulated miRs in GSE102286 and miRs that target Rad51 as predicted by TargetScan and ENCORI. C RT-qPCR was used to detect the gene expression level of miR-130a-3p in cells upon different treatments. D ChIP was used to detect the RNA pol II binding in miR-130a-3p promoter region. E ChIP was used to detect the binding of AcH4 in miR-130a-3p promoter region. F ChIP was used to detect the binding of HDAC2 in miR-130a-3p promoter region. G RT-qPCR was used to detect the gene expression levels of HDAC2 and miR-130a-3p. H MTT assay was used to detect the viability of cells upon different treatments. I Transwell assay was used to detect the migration and invasion of cells upon different treatments. J Flow cytometry was used to detect the apoptosis of cells upon different treatments. *p < 0.05. **p < 0.01. ***p < 0.001. ****p < 0.0001. Data between two groups were compared by unpaired t test, and those among multiple groups were compared by one-way ANOVA followed by Tukey’s post hoc tests. Data among multiple groups at different time points were compared by repeated measures ANOVA, followed by Bonferroni post hoc tests. Cellular experiments were repeated three times

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