Additional file 2: of Landscape of tumor suppressor long noncoding RNAs in breast cancer

Figure S1. TSLNR expression in breast cancer samples and normal tissue samples in HMUCC. Figure S2. Genetic alteration was also examined for these lncRNAs in breast cancer data in TCGA. Figure S3. A&B Patients with high expression (N = 266) of TSLNRs (ACVR2B-AS1 and WEE2-AS1) had favorable OS than those with low expression (N = 266) in breast cancer in TCGA. C-F Patients with high expression (N = 266) of TSLNRs (ACVR2B-AS1, WEE2-AS1, LINC-PINT and HAND2-AS1) had favorable DFS than those with low expression (N = 266) in breast cancer in TCGA. Figure S4. A-D Patients with high expression (N = 266) of TSLNRs (CYP1B1-AS1, LINC-PINT, LINC00667 and GRIK1-AS1) had favorable OS than those with low expression (N = 266) in breast cancer in TCGA. E-G Patients with high expression (N = 266) of TSLNRs (CYP1B1-AS1, FAM66C and GRIK1-AS1) had favorable DFS than those with low expression (N = 266) in breast cancer in TCGA. Figure S5. EPB41L4A-AS2 was downregulated in MDA-MB-231 breast cancer cells with ZNF217 overexpression in GEO dataset GSE35511. Figure S6. A Overlapping genes of EPB41L4A-AS2 correlated genes and paclitaxel related genes in BETMAN-TCM. B KEGG pathway analysis for EPB41L4A-AS2 correlated genes in BETMAN-TCM. C GO analysis for EPB41L4A-AS2 correlated genes in BETMAN-TCM.D OMIM analysis for EPB41L4A-AS2 correlated genes in BETMAN-TCM.E Pharmacological network analysis indicates that EPB41L4A-AS2 may be involved in paclitaxel related process in breast cancer. F Pharmacological network analysis indicates that EPB41L4A-AS2 may be involved in crosstalk with paclitaxel related genes in breast cancer. Figure S7. A Expression of EPB41L4A-AS2 in breast cancer cell lines. B&C overexpression efficiency of EPB41L4A-AS2 in UACC812 and BT549 cells. D Knockdown efficiency of EPB41L4A-AS2 in MDA-MB-453 cells. Figure S8. A-C Overexpression of each lncRNA (MEG3, WEE2-AS1 and HAND2-AS1) inhibited clone formation in UACC812 cells. D-F Overexpression of each lncRNA (MEG3, WEE2-AS1 and HAND2-AS1) inhibited cell viability in UACC812 cells. (ZIP 19903 kb)

图S1：HMUCC队列乳腺癌样本与正常组织样本中TSLNR的表达水平。
图S2：针对癌症基因组图谱（The Cancer Genome Atlas, TCGA）乳腺癌数据集内的上述长链非编码RNA（long non-coding RNA, lncRNA），本研究检测了其遗传变异情况。
图S3：A、B 在TCGA乳腺癌队列中，TSLNR家族成员ACVR2B-AS1与WEE2-AS1高表达组（N=266）的总生存期（Overall Survival, OS）显著优于低表达组（N=266）；C-F 该队列中，TSLNR家族成员ACVR2B-AS1、WEE2-AS1、LINC-PINT及HAND2-AS1高表达组（N=266）的无病生存期（Disease-Free Survival, DFS）显著优于低表达组（N=266）。
图S4：A-D 在TCGA乳腺癌队列中，TSLNR家族成员CYP1B1-AS1、LINC-PINT、LINC00667及GRIK1-AS1高表达组（N=266）的总生存期显著优于低表达组（N=266）；E-G 该队列中，TSLNR家族成员CYP1B1-AS1、FAM66C及GRIK1-AS1高表达组（N=266）的无病生存期显著优于低表达组（N=266）。
图S5：在基因表达综合数据库（Gene Expression Omnibus, GEO）数据集GSE35511中，过表达ZNF217的MDA-MB-231乳腺癌细胞内EPB41L4A-AS2表达显著下调。
图S6：A BETMAN-TCM数据库中EPB41L4A-AS2关联基因与紫杉醇相关基因的交集基因；B 针对BETMAN-TCM数据库中EPB41L4A-AS2关联基因的京都基因与基因组百科全书（Kyoto Encyclopedia of Genes and Genomes, KEGG）通路富集分析；C 针对BETMAN-TCM数据库中EPB41L4A-AS2关联基因的基因本体论（Gene Ontology, GO）富集分析；D 针对BETMAN-TCM数据库中EPB41L4A-AS2关联基因的在线人类孟德尔遗传（Online Mendelian Inheritance in Man, OMIM）分析；E 药理学网络分析显示，EPB41L4A-AS2可能参与乳腺癌中紫杉醇相关生物学过程；F 药理学网络分析显示，EPB41L4A-AS2可能参与乳腺癌中与紫杉醇相关基因的交叉调控。
图S7：A EPB41L4A-AS2在各乳腺癌细胞系中的表达水平；B、C EPB41L4A-AS2在UACC812与BT549细胞中的过表达验证效率；D EPB41L4A-AS2在MDA-MB-453细胞中的敲低验证效率。
图S8：A-C 在UACC812细胞中过表达MEG3、WEE2-AS1或HAND2-AS1任一长链非编码RNA，均可抑制细胞克隆形成能力；D-F 在UACC812细胞中过表达MEG3、WEE2-AS1或HAND2-AS1任一长链非编码RNA，均可降低细胞活力。（压缩包大小：19903 kb）