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Transcriptomic analysis of SKM1 cells treated with APR-246 (APR), 5-Azacytidine (AZA) or both (APR-AZA)

ABSTRACT: Transcriptomic analysis of SKM1 cells treated with APR-246 (APR), 5-Azacytidine (AZA) or both (APR-AZA)

PROVIDER: PRJNA433156 | ENA |

REPOSITORIES: ENA

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Transcriptomic analysis of SKM1 cells treated with APR-246 (APR), 5-Azacytidine (AZA) or both (APR-AZA)

Project description:In order to explain the synergistic effects observed by the combination APR+AZA in MDS cells by synergistic activated pathways, we performed a transcriptomic analysis of MDS cells treated with each drug alone and compared it to the combination.

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APR-246 enhances colorectal cancer sensitivity to radiotherapy

Project description:p53 mutation is common and highly related to radiotherapy resistance in rectal cancer. APR-246, as a small molecule, can restore the tumor-suppressor function to mutant p53. There is no study on combining APR-246 with radiation in rectal cancer; therefore, we examined whether APR-246 sensitized colorectal cancer cells with different p53 status to radiation. The combination treatment had synergistic effects on HCT116p53-R248W/-(p53Mut) cells, followed by HCT116p53+/+(p53WT) cells, and exhibited an additive effect on HCT116p53-/-(p53Null) cells through inhibiting proliferation, enhancing reactive oxygen species, and apoptosis. The results were confirmed in zebrafish xenografts. Comparison of the transcriptome in colorectal cancer cells with different p53 status 72hrs post-treatment with APR-246, irradiation, or the combination of APR-246 with irradiation was carried out. p53Mut and p53WT cells shared more activated pathways and differentially expressed genes following the combination treatment, compared to p53Null cells, although the combination treatment regulated individual pathways in the different cell lines. APR-246 mediated radio-sensitization effects through p53-dependent and -independent ways.

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Ovarian cancers with low CIP2A tumor expression constitute an APR-246 sensitive disease subtype

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Variability in functional p53 reactivation by Prima-1Met/APR-246 in Ewing sarcoma

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