Additional file 2: of PIWI-interacting RNA-36712 restrains breast cancer progression and chemoresistance by interaction with SEPW1 pseudogene SEPW1P RNA

Figure S1. Downregulation of piR-36,712 in breast cancer. Figure S2. Effects of piR-36,712 on malignant phenotypes of breast cancer cells. Figure S3. Effects of piR-36,712 on expressions of nearby genes and sequence alignment of SEPW1P and piR-36,712 and SEPW1. Figure S4. Analysis of the shared target miRNAs between SEPW1P and SEPW1. Figure S5. Effects of altering expression of SEPW1P, SEPW1 or P53 on oncogenic functions of piR-36,712. Figure S6. Ectopic piR-36,712 expression suppresses the phenotypes of breast cancer cells in a P53 dependent maner regardless molecular subtype. Figure S7. Ectopic piR-36,712 expression influences IC50 of paclitaxel and doxorubicin on MCF7 and ZR75â 1 cells. Figure S8. Ectopic piR-36,712 expression influences IC50 of paclitaxel and doxorubicin on breast cancer cells in a P53 dependent maner regardless molecular subtype. Figure S9. Proposed acting model for the tumor suppressor role of piR-36,712 in breast cancer. (ZIP 21746 kb)

图S1. 乳腺癌中piR-36,712的表达下调。
图S2. piR-36,712对乳腺癌细胞恶性表型的影响。
图S3. piR-36,712对邻近基因表达水平的调控作用，以及硒蛋白W假基因1（SEPW1P）、piR-36,712与硒蛋白W（SEPW1）的序列比对。
图S4. SEPW1P与SEPW1共享的靶微小RNA（miRNAs）的分析。
图S5. 改变SEPW1P、SEPW1或P53的表达水平对piR-36,712致癌功能的影响。
图S6. 异位表达piR-36,712可通过P53依赖的方式抑制乳腺癌细胞的表型，且该作用不受癌细胞分子亚型的影响。
图S7. 异位表达piR-36,712对MCF7与ZR75-1细胞的紫杉醇与阿霉素半数抑制浓度（IC50）的影响。
图S8. 异位表达piR-36,712可通过P53依赖的方式影响乳腺癌细胞对紫杉醇与阿霉素的IC50，且该作用不受癌细胞分子亚型的影响。
图S9. piR-36,712在乳腺癌中发挥抑癌作用的拟议作用模型。（压缩包大小：21746 kb）