| Autor: |
Toshiyasu Taniguchi, Christopher J. Kemp, Muneesh Tewari, Patrick S. Mitchell, Emily Villegas, Philamer Calses, Kiranjit K. Dhillon, Yemin Wang, Jen-Wei Huang |
| Rok vydání: |
2023 |
| DOI: |
10.1158/1541-7786.22510426.v1 |
| Popis: |
PDF file - 2066K, S1. MiR-103 and miR-107 inhibit DNA damage-induced RAD51 foci formation in cancer cells. S2. MiR-103 and miR-107 promote chemosensitivity in U2OS cells. S3. MiR-103 and miR-107 promote chemosensitivity to cisplatin and a PARP inhibitor in HeLa and PEO1 C4-2 cells. S4. MiR-107 promotes chemosensitivity in H1299, HeLa and PEO1 C4-2 cells. S5. MiR-103 and miR-107 regulate RAD51 and RAD51D. S6. RAD51 is critical for cellular resistance to cisplatin and a PARP inhibitor. S7. RAD51 downregulation is critical for miR-103/107-mediated regulation of HR. S8. RAD51D downregulation is relevant to miR-103/107-mediated chemosensitivity. S9. Inhibition of miR-103 and miR-107 mildly de-represses RAD51D expression. S10. MiR-103 and miR-107 are inversely correlated with RAD51D mRNA expression in several tumor subtypes. Table S1. Summary of library screening to identify microRNAs that regulate IR-induced RAD51 foci formation. Table S2. Correlation between miR-103 or miR-107 and target gene expression in the NCI-60 panel of cancer cell lines. Table S3. Correlation between miR-103 or miR-107 and target gene expression in several tumor subtypes from TCGA. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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