Research Paper Volume 16, Issue 1 pp 226—245

Figure 1. Comprehensive landscape of RBMX. (A) Transcriptional expression levels of RBMX in cancer based on TCGA and GTEx cohorts. (B) Different expression levels of RBMX between CHOL and normal cholecyst tissues. (C) Analysis of RBMX alteration frequency in different types of cancer using data from the cBioPortal database. (D) Pearson correlations between RBMX expression and RBMX copy number variation in each type of cancer. (E) Pearson correlations between RBMX expression and RBMX transcriptional start site (TSS) methylation in each type of cancer. (F) Immunofluorescence images of RBMX protein, nucleus, endoplasmic reticulum (ER), microtubules, and merged images in MCF7 and U2-OS cell lines. (G) The protein–protein interaction (PPI) network displayed interaction between the proteins and RBMX. (H–M) RBMX expression between clinical tumor samples and related normal samples in CHOL (H, I), LIHC (J, K), and GBM (L, M). CHOL, cholangiocarcinoma; GBM, glioblastoma; GTEx, Genotype-Tissue Expression; LIHC, liver hepatocellular carcinoma; RBMX, RNA binding motif protein X-linked; TCGA, The Cancer Genome Atlas.