ArticleClinical and experimental medicine2026
Novel antagonist APG-115 targets MDM2-p53 to induce p53-mediated apoptosis and radiosensitization in colorectal cancer.
Article in Clinical and experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Colorectal cancer remains a major global health burden, and treatment outcomes for advanced disease are still unsatisfactory. APG-115 is a next-generation small-molecule MDM2 inhibitor developed in China that restores wild-type p53 activity. However, its therapeutic potential in colorectal cancer has not been fully explored. APG-115's impact on colorectal cancer cells was evaluated through CCK-8 assays and AnnexinV-FITC/PI staining. The dependence of APG-115 activity on p53 status was assessed in p53-knockdown cell lines. In vivo, the antitumor efficacy and radiosensitizing effects of APG-115 were evaluated in nude-mouse xenograft models. APG-115 exerted a potent inhibitory effect on the proliferation of p53 wild-type colorectal cancer cell lines LOVO, RKO, and HCT116, while showed no significant impact on p53-mutant lines. In wild-type cells, APG-115 induced apoptosis in a dose-dependent manner and caused G0/G1 cell-cycle arrest. APG-115 significantly upregulated p53 and its downstream targets (MDM2, p21, PUMA), whereas these effects were absent in p53-mutant or p53-knockdown cells. In vivo, APG-115 suppressed RKO tumor growth in a dose-dependent manner, accompanied by increased p53, MDM2 and p21 expression and reduced Ki-67. Immunofluorescence further confirmed enhanced apoptosis following treatment. Importantly, the combination of APG-115 with radiotherapy significantly promoted apoptosis, decreased the S-phase proportion, and increased G2-phase arrest in p53 wild-type cells. Radiosensitization was abolished in p53-knockout RKO xenografts, confirming the requirement of an intact MDM2-p53 pathway. APG-115 effectively inhibits proliferation, induces apoptosis, and enhances radiosensitivity in p53 wild-type colorectal cancer. These findings support APG-115 as a promising therapeutic candidate for colorectal cancers retaining functional p53.
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