Evidence map›Paper›PMID 40627200›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2026

Ononin induces ferroptosis in colorectal cancer cells via the PI3K/AKT/Nrf2 pathway to enhance anti-cancer immunotherapy.

Yang Gui, Shuangjiao Deng, Jingjing Li, Dongmei Zuo, Heng Fan

Abstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. FAT4 loss promotes tumor growth and ferroptosis resistance in hepatocellular carcinoma via PI3K/AKT pathway activation.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  2. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Yang Gui *Department of Integrated Traditional Chinese and Western Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Shuangjiao Deng *Department of Integrated Traditional Chinese and Western Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Jingjing LiDepartment of Integrated Traditional Chinese and Western Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Dongmei ZuoDepartment of Integrated Traditional Chinese and Western Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. ZUO_345@126.com.
Heng FanDepartment of Integrated Traditional Chinese and Western Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. 2003xh0803@hust.edu.cn.

Funding

National Natural Science Foundation of China 81774093National Natural Science Foundation of China 81904018National Natural Science Foundation of China 82205058Research Collaboration Project of Huazhong University of Science and Technology Union Jingshan Hospital 2023-XHJS-008
6 · The paper itself

Abstract

Colorectal cancer (CRC) represents one of the most prevalent forms of malignant neoplasms affecting the digestive tract. Recent studies have demonstrated that the induction of ferroptosis in tumor cells represents a novel therapeutic strategy. Ononin, an isoflavone glycoside compound derived from traditional Chinese medicinal plants, has garnered attention for its purported therapeutic efficacy. This study integrated network pharmacology and experimental studies to elucidate the underlying mechanism involved in the therapeutic action of ononin against CRC. The results demonstrated that ononin induced lipid peroxidation and a reduction in mitochondrial membrane potential (MMP), indicative of mitochondrial damage in CRC cells, accompanied by a pronounced decline in GPX4 expression. The combination of ononin and anti-PD-L1 therapy demonstrated a notable enhancement in tumor growth inhibition in the MC38 mouse CRC model, accompanied by a marked increase in the proportion of intratumoral IFNγ

Indexed as

Colorectal NeoplasmsFerroptosisAnimalsB7-H1 AntigenCell Line, TumorHumansImmune Checkpoint InhibitorsImmunotherapyMembrane Potential, MitochondrialMiceMice, Inbred BALB CNF-E2-Related Factor 2Phosphatidylinositol 3-KinasesPhospholipid Hydroperoxide Glutathione PeroxidaseProto-Oncogene Proteins c-aktSignal TransductionB7-H1 AntigenImmune Checkpoint InhibitorsNFE2L2 protein, humanNfe2l2 protein, mouseNF-E2-Related Factor 2Phosphatidylinositol 3-KinasesPhospholipid Hydroperoxide Glutathione PeroxidaseProto-Oncogene Proteins c-aktColorectal cancerFerroptosisImmunotherapyOnoninPI3K/AKT/Nrf2 pathway

Identifiers

PMID40627200

What OpenQuestion holds

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Registered trials

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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.