Additional File 2 of A Novel Trna-Derived Fragment AS-tDR-007333 Promotes the Malignancy of NSCLC Via the HSPB1/MED29 and ELK4/MED29 Axes

Additional file 2: Figure S1. Characteristics of AS-tDR-007333. Figure S2. The transfection efficiencies of mimics, plasmids, and si-RNAs in NSCLC cells. Figure S3. AS-tDR-007333 did not affect apoptosis phenotypes in NSCLC cells. Figure S4. Gene set enrichment analysis (GSEA) of AS-tDR-007333-treated cells. Figure S5. In silico analysis of MED29 in NSCLC based on TCGA database. Figure S6. AS-tDR-007333 regulates MED29 expression and functionally interacts with MED29 in NSCLC cells. Figure S7. HSPB1 is up-regulated in NSCLC (in silico analysis based on TCGA database). Figure S8. CHX-chase assay results suggested that AS-tDR-007333 may not affect HSPB1 protein degradation. Figure S9. ELK4 was up-regulated in NSCLC based on TCGA database. Figure S10. ELK4 was up-regulated in NSCLC cells. Figure S11. Schematic diagram of genomic organization and chromatin state of the human MED29 gene locus. Figure S12. Overview of AS-tDR-007333 staining in tissue microarrays (TMAs) spots. Figure S13. AS-tDR-007333 inhibitor did not affect the body weight different subgroups of rats during the period of experiments. Figure S14. Correlations between AS-tDR-007333 and HSPB1, ELK4, and MED29 in NSCLC tumor tissues.