ArticleCancer cell international2026
APX3330 reverses the immunosuppressive tumor microenvironment during colorectal carcinogenesis.
Article in Cancer cell international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- APE1/Ref-1: multifunctional biology, selective inhibition, and the path to clinical translation.Expert opinion on therapeutic targets · 2026Review
- Myeloid-derived suppressor cells in colorectal cancer: mechanisms of immunosuppression, therapy resistance and therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
BACKGROUND AND
objectivesColorectal cancer (CRC) ranks as the third most common cancer globally and is the second leading cause of cancer-related deaths. While some CRC patients with deficient mismatch repair (dMMR) or high microsatellite instability (MSI-H) respond to immune checkpoint inhibitors (ICIs), many exhibit resistance, partly due to polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs). APE1/Ref-1, a bifunctional protein involved in DNA repair and redox regulation, has an inhibitor, APX3330, which targets its redox function without affecting DNA repair. This study aims to explore the relationship between APE1/Ref-1 and PMN-MDSCs in CRC, assess the impact of APX3330 on the tumor microenvironment (TME), and identify a novel therapeutic target.
methodsSurgical specimens from 176 CRC patients were analyzed using immunohistochemistry (IHC) and multiplex IHC (mIHC) to evaluate APE1/Ref-1 expression, tumor stage, malignancy grade, and immune cell infiltration. An azoxymethane/dextran sodium sulfate (AOM/DSS) model was established to simulate murine colon cancer. RNA sequencing (RNA-seq) and mIHC were employed to examine the effects of APX3330 on immune cell infiltration. Additionally, MC38 murine colon cancer cells were used to establish subcutaneous tumors in mice to analyze the impact of APX3330 and APE1/Ref-1 on immune cell infiltration.
resultsElevated APE1/Ref-1 expression in CRC was associated with increased PMN-MDSC infiltration. APX3330 modulated the TME by regulating PMN-MDSCs and enhancing the infiltration of CD4+ and CD8+ T cells, thereby altering the immune landscape. APX3330 demonstrated enhanced efficacy in tumors with low APE1/Ref-1 expression, and downregulated genes associated with APX3330 were linked to poorer prognosis.
conclusionsIncreased APE1/Ref-1 expression in CRC patients correlates with worse clinical outcomes and heightened PMN-MDSC infiltration. APX3330 effectively reshapes the TME by altering immune cell infiltration, highlighting its potential as a therapeutic agent for CRC.
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