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- W4385458217 abstract "<div>Abstract<p>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. As there is currently no existing study on combining APR-246 with radiation in rectal cancer, our objective was to investigate whether APR-246 could enhance the sensitivity of colorectal cancer cells, regardless of their p53 status, to radiation treatment. The combination treatment had synergistic effects on HCT116<sup>p53-R248W/−</sup> (p53Mut) cells, followed by HCT116<sup>p53+/+</sup> [wild-type p53 (p53WT)] cells, and exhibited an additive effect on HCT116<sup>p53−/−</sup> (p53Null) cells through inhibiting proliferation, enhancing reactive oxygen species, and apoptosis. The results were confirmed in zebrafish xenografts. Mechanistically, p53Mut and p53WT cells shared more activated pathways and differentially expressed genes following the combination treatment, compared with p53Null cells, although the combination treatment regulated individual pathways in the different cell lines. APR-246 mediated radiosensitization effects through p53-dependent and -independent ways. The results may provide evidence for a clinical trial of the combination in patients with rectal cancer.</p></div>" @default.
- W4385458217 created "2023-08-02" @default.
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- W4385458217 date "2023-08-01" @default.
- W4385458217 modified "2023-09-27" @default.
- W4385458217 title "Data from APR-246 Enhances Colorectal Cancer Sensitivity to Radiotherapy" @default.
- W4385458217 doi "https://doi.org/10.1158/1535-7163.c.6769274.v1" @default.
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