Evidence map›Paper›PMID 41739401›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2026

Apigenin 7-glucoside reprograms tumor metabolism and enhances immunotherapy efficacy in colorectal cancer via DLX5.

Guijun Zou, Yiwei Jiang, Rui Ma, Songyan Li, Chaojun Zhang

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Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 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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5 · Who and what money

Authors and funding

5 authors.

Guijun Zou *Department of General Surgery, The First Medical Center of Chinese PLA General Hospital, Beijing, 100853, China.
Yiwei Jiang *Department of General Surgery, The First Medical Center of Chinese PLA General Hospital, Beijing, 100853, China.
Rui Ma *Department of General Surgery, The First Medical Center of Chinese PLA General Hospital, Beijing, 100853, China.
Songyan LiDepartment of General Surgery, The First Medical Center of Chinese PLA General Hospital, Beijing, 100853, China. lisongyan301@163.com.
Chaojun ZhangDepartment of General Surgery, The First Medical Center of Chinese PLA General Hospital, Beijing, 100853, China. zcjdlyxzx@163.com.ORCID http://orcid.org/0000-0002-6898-7257

Funding

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6 · The paper itself

Abstract

backgroundThe progression of colorectal cancer (CRC) is closely associated with glycolysis, angiogenesis and immune response. While the natural flavonoid Apigenin 7-glucoside (A7G) exhibits anti-tumor potential, its effects on these three processes remain unclear. This study aims to investigate the impact of A7G on the CRC landscape and to assess its synergistic effect when combined with PD-1 inhibitors.

methodsWestern blotting was used to detect the effect of A7G on glycolysis and angiogenesis-related factors. Immunohistochemistry and flow cytometry were employed to analyze changes in the tumor immune microenvironment. The CT26 mouse xenograft model with overexpressed DLX5 was established to evaluate the role of A7G in modulating metabolic and immune responses. Finally, the therapeutic effect of A7G in combination with PD-1 inhibitors was explored.

resultsA7G significantly decreased the expression of glycolysis and angiogenesis-related factors, a process partially reversed by DLX5 overexpression. Flow cytometry analysis showed that A7G treatment increased the ratio of CD4⁺ T cells/CD8⁺ T cells and reduced the infiltration of M2 macrophages and Treg cells, which was also modulated by DLX5. When combined with PD-1 inhibitors, A7G markedly suppressed tumor growth and enhanced the efficacy of immune therapy.

conclusionA7G treatment demonstrated potential anti-tumor activity in CRC, which is characterized by the simultaneous attenuation of glycolysis and immune evasion via the DLX5 axis. When used in combination with PD-1 inhibitors, A7G significantly enhances the effects of immunotherapy, providing a novel strategy for cancer treatment.

Indexed as

ApigeninColorectal NeoplasmsHomeodomain ProteinsImmunotherapyTranscription FactorsAnimalsCell Line, TumorDrug SynergismFemaleGlycolysisHumansImmune Checkpoint InhibitorsMetabolic ReprogrammingMiceMice, Inbred BALB CNeovascularization, PathologicApigeninHomeodomain ProteinsImmune Checkpoint InhibitorsTranscription FactorsColorectal cancerGlycolysisTumor immune microenvironment

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.