Additional file 1: of P53-R273H mutation enhances colorectal cancer stemness through regulating specific lncRNAs
Creators: name: Zhao, Yuechao
name: Li, Yiran
name: Sheng, Jie
name: Wu, Fan
name: Li, Kai
name: Huang, Rong
name: Wang, Xiaojuan
name: Jiao, Tao
name: Guan, Xin
name: Lu, Yan
name: Chen, Xiao
name: Luo, Zhiwen
name: Zhou, Yanchi
name: Hu, Hanjie
name: Liu, Wenjie
name: Du, Boyu
name: Miao, Shiying
name: Cai, Jianqiang
name: Wang, Linfang
name: Zhao, Hong
name: Ying, Jianming
name: Bi, Xinyu
name: Song, Wei
Publisher: name: figshare
Year: 2019
Subjects: subject: Biochemistry
subject: Medicine
subject: Cell Biology
subject: Genetics
subject: FOS: Biological sciences
subject: Molecular Biology
subject: Biological Sciences not elsewhere classified
subject: Developmental Biology
subject: Cancer
subject: Hematology
subject: Computational Biology

description: Figure S1A. Western blot analysis of HCT116 p53−/− over-expression p53 point mutants. Figure S2A. Schematic diagram of constructing HCT116 endogenous p53 point mutant (PM) cells. Figure S2B. Sanger sequencing of p53-R273H point mutant (R273H PM) representative cells. Figure S3. Global profiling and identification of p53-R273H-regulated lncRNAs. Figure S3A. Different types of transcripts. Figure S3B. Different types of noncoding transcripts. Figure S3C. A two-dimensional heatmap of 1957 lncRNAs. Figure S3D. Principal components analysis (PCA) for three independent replicates. The principal component accounted of p53-R273H and p53-ctrl were 85.7 and 69.6% respectively. Figure S4A. Validation of differentially expressed 41 lncRNAs by RT-qPCR. Figure S5. Genome-wide analysis of p53-R273H-regulated protein coding genes in CSC state. Figure S5A. A two-dimensional heatmap of 307 mRNAs. Figure S5B. Principal components analysis (PCA) for three independent replicates. Figure S5C. Hierarchical clustering for three independent replicates. Figure S5D. Signaling pathway based on KEGG enrichment analysis of p53-R273H-regulated coding genes in CSC state. Figure S5E. GO biological processes enrichment analysis of p53-R273H-regulated coding genes in CSC state. Figure S5F. Regulatory network construction of TFs (dark blue), lncRNAs (red) and mRNAs (light green). The average degree of lncRNAs was 46.39, higher than 35.39, the average degree of protein coding genes. Figure S6A. ChIP-qPCR for validating of the binding of p53 and the promotor of lnc273–31 or lnc273–34. Figure S6B. The expression levels in ALDH positive and ALDH negative cells sorted by FACS. Figure S6C. Subcellular localization of lnc273–31 and lnc273–34 was analyzed by RT-qPCR upon biochemical fractionation of p53-R273H speroid cells. Figure S7A. Quantitative real-time PCR analyzed the expression of stemness-related genes in HCT116 p53 PM cells. Figure S7B. Western blot analysis of ZEB1 and snail in lnc273–31 or lnc273–34 depletion cells. Figure S8. The association of age (S8A), gender (S8B), smoking (S8C), alcohol abuse (S8D), family history (S8E), lymphatic vessel (S8F), TNM stage (S8G-I) and the expression levels of lncRNAs in 25 colorectal cancer patients with or without p53-R273H mutation. Table S1. Primers for qPT-PCR. Table S2. Purchased ASO pool sequences. Table S3. Primers for ChIP-qPCR. (DOCX 2058 kb)