Evidence map›Paper›PMID 41493849›Full record

ArticlePhytotherapy research : PTR2026

Calycosin Targets the CYP1B1-AKT/SP1-GPX4 Axis to Modulate Ferroptosis in Colorectal Carcinogenesis.

Lihan Bie, Xin Lei, Di Wu, Yang Zhang, Chengshan He, Luyao Liu, Jiawei Zhou, Xin Zhou, Yingying Lu, Zheng Xu

Abstract read
In one paragraph

Article in Phytotherapy research : PTR, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

10 authors.

Lihan BieDepartment of Clinical Laboratory, Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Xin LeiDepartment of Clinical Laboratory, Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Di WuDepartment of Clinical Laboratory, Yangpu Hospital, School of Medicine, Tongji University, Shanghai, People's Republic of China.
Yang ZhangDepartment of Clinical Laboratory, Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Chengshan HeDepartment of Clinical Laboratory, Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.ORCID https://orcid.org/0009-0006-2503-5308
Luyao LiuDepartment of Clinical Laboratory, Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Jiawei ZhouSchool of Medicine, Anhui University of Science and Technology, Huainan, Anhui, People's Republic of China.
Xin ZhouSchool of Medicine, Anhui University of Science and Technology, Huainan, Anhui, People's Republic of China.
Yingying LuDepartment of Clinical Laboratory, Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Zheng XuDepartment of Clinical Laboratory, Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.ORCID https://orcid.org/0009-0000-4015-8898

Funding

The Scientific Research Program of Shanghai Pudong New Area Health Commission PW2022A-22
6 · The paper itself

Abstract

Calycosin, a natural flavonoid small-molecule compound derived from traditional Chinese medicine, has demonstrated remarkable pharmacological activity in the field of cancer therapy. This study systematically elucidates the molecular mechanisms of Calycosin in colorectal cancer (CRC) treatment through integrated in vivo and in vitro experiments. In vivo experiments revealed that Calycosin effectively inhibits subcutaneous tumor growth in CRC-bearing mice. In vitro assays and transcriptome sequencing confirmed that Calycosin effectively suppresses migration, invasion, epithelial-mesenchymal transition (EMT), and induces ferroptosis in human CRC cells, thereby inhibiting malignant tumor behaviors. Cellular Thermal Shift Assay (CETSA) and site-directed mutagenesis experiments first identified cytochrome P450 1B1 (CYP1B1) and Gly-329 as critical binding targets and sites for Calycosin. Functional studies showed that CYP1B1 knockdown in vitro and in vivo suppresses GPX4 expression and enhances ferroptosis in CRC cells. Mechanistically, CYP1B1 activates the AKT/SP-1 signaling pathway to upregulate GPX4 expression, thereby modulating colorectal carcinogenesis and progression. In summary, this study first unveils the crucial role of Calycosin and the CYP1B1-AKT/SP1-GPX4 regulatory axis in CRC ferroptosis, providing novel theoretical foundations for targeted therapy using traditional Chinese medicine-derived small molecules against colorectal cancer.

Indexed as

Colorectal NeoplasmsCytochrome P-450 CYP1B1FerroptosisIsoflavonesPhospholipid Hydroperoxide Glutathione PeroxidaseAnimalsCarcinogenesisCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionHumansMiceMice, Inbred BALB CMice, NudeProto-Oncogene Proteins c-aktSignal Transduction7,3'-dihydroxy-4'-methoxyisoflavoneCYP1B1 protein, humanCytochrome P-450 CYP1B1IsoflavonesPhospholipid Hydroperoxide Glutathione PeroxidaseProto-Oncogene Proteins c-aktCalycosinCRCCYP1B1ferroptosisGPX4

Identifiers

PMID41493849
PMCPMC12879287

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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.