Evidence map›Paper›PMID 38684798›Full record

ArticleActa pharmacologica Sinica2024

Baicalein triggers ferroptosis in colorectal cancer cells via blocking the JAK2/STAT3/GPX4 axis.

Jian-Qin Lai, Le-le Zhao, Chao Hong, Qiu-Ming Zou, Jin-Xuan Su, Si-Jia Li, Xiao-Feng Zhou, Zi-Sheng Li, Bo Deng, Jie Cao and 1 more

Abstract read
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Article in Acta pharmacologica Sinica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 2 pooled it
–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

55 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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  6. The Emerging Role of Ferroptosis in Pediatric Cancer Biology and Therapy.International journal of molecular sciences · 2026
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  18. Ononin combined withBiochemistry and biophysics reports · 2026
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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

11 authors.

Jian-Qin Lai *Department of General Surgery, The First Affiliated Hospital of Jinan University, Jinan University, Guangzhou, 510630, China.
Le-le Zhao *State Key Laboratory of Bioactive Molecules and Drug ability Assessment; MOE Key Laboratory of Tumor Molecular Biology; Department of Pharmacology, School of Medicine, Jinan University, Guangzhou, 510632, China.
Chao Hong *State Key Laboratory of Bioactive Molecules and Drug ability Assessment; MOE Key Laboratory of Tumor Molecular Biology; Department of Pharmacology, School of Medicine, Jinan University, Guangzhou, 510632, China.
Qiu-Ming ZouState Key Laboratory of Bioactive Molecules and Drug ability Assessment; MOE Key Laboratory of Tumor Molecular Biology; Department of Pharmacology, School of Medicine, Jinan University, Guangzhou, 510632, China.
Jin-Xuan SuState Key Laboratory of Bioactive Molecules and Drug ability Assessment; MOE Key Laboratory of Tumor Molecular Biology; Department of Pharmacology, School of Medicine, Jinan University, Guangzhou, 510632, China.
Si-Jia LiState Key Laboratory of Bioactive Molecules and Drug ability Assessment; MOE Key Laboratory of Tumor Molecular Biology; Department of Pharmacology, School of Medicine, Jinan University, Guangzhou, 510632, China.
Xiao-Feng ZhouState Key Laboratory of Bioactive Molecules and Drug ability Assessment; MOE Key Laboratory of Tumor Molecular Biology; Department of Pharmacology, School of Medicine, Jinan University, Guangzhou, 510632, China.
Zi-Sheng LiState Key Laboratory of Bioactive Molecules and Drug ability Assessment; MOE Key Laboratory of Tumor Molecular Biology; Department of Pharmacology, School of Medicine, Jinan University, Guangzhou, 510632, China.
Bo DengThe Affiliated Shunde Hospital of Jinan University, Foshan, 528305, China. gzyybird@aliyun.com.
Jie CaoDepartment of General Surgery, The First Affiliated Hospital of Jinan University, Jinan University, Guangzhou, 510630, China. eycaojie@scut.edu.cn.
Qi QiState Key Laboratory of Bioactive Molecules and Drug ability Assessment; MOE Key Laboratory of Tumor Molecular Biology; Department of Pharmacology, School of Medicine, Jinan University, Guangzhou, 510632, China. qiqikc@jnu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is a prevalent form of gastrointestinal malignancy with challenges in chemotherapy resistance and side effects. Effective and low toxic drugs for CRC treatment are urgently needed. Ferroptosis is a novel mode of cell death, which has garnered attention for its therapeutic potential against cancer. Baicalein (5, 6, 7-trihydroxyflavone) is the primary flavone extracted from the dried roots of Scutellaria baicalensis that exhibits anticancer effects against several malignancies including CRC. In this study, we investigated whether baicalein induced ferroptosis in CRC cells. We showed that baicalein (1-64 μM) dose-dependently inhibited the viability of human CRC lines HCT116 and DLD1. Co-treatment with the ferroptosis inhibitor liproxstatin-1 (1 μM) significantly mitigated baicalein-induced CRC cell death, whereas autophagy inhibitor chloroquine (25 μM), necroptosis inhibitor necrostatin-1 (10 μM), or pan-caspase inhibitor Z-VAD-FMK (10 μM) did not rescue baicalein-induced CRC cell death. RNA-seq analysis confirmed that the inhibitory effect of baicalein on CRC cells is associated with ferroptosis induction. We revealed that baicalein (7.5-30 μM) dose-dependently decreased the expression levels of GPX4, key regulator of ferroptosis, in HCT116 and DLD1 cells by blocking janus kinase 2 (JAK2)/STAT3 signaling pathway via direct interaction with JAK2, ultimately leading to ferroptosis in CRC cells. In a CRC xenograft mouse model, administration of baicalein (10, 20 mg/kg, i.g., every two days for two weeks) dose-dependently inhibited the tumor growth with significant ferroptosis induced by inhibiting the JAK2/STAT3/GPX4 axis in tumor tissue. This study demonstrates that ferroptosis contributes to baicalein-induced anti-CRC activity through blockade of the JAK2/STAT3/GPX4 signaling pathway, which provides evidence for the therapeutic application of baicalein against CRC.

Indexed as

Colorectal NeoplasmsFerroptosisFlavanonesJanus Kinase 2Phospholipid Hydroperoxide Glutathione PeroxidaseSTAT3 Transcription FactorAnimalsCell Line, TumorCell SurvivalDose-Response Relationship, DrugHCT116 CellsHumansMiceMice, Inbred BALB CMice, NudeSignal TransductionbaicaleinFlavanonesJAK2 protein, humanJanus Kinase 2Phospholipid Hydroperoxide Glutathione PeroxidaseSTAT3 protein, humanSTAT3 Transcription Factorbaicaleincolorectal cancerferroptosisGPX4JAK2/STAT3liproxstatin-1

Identifiers

PMID38684798
PMCPMC11272787

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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.