Evidence map›Paper›PMID 39475053›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

Targeting BRIX1 via Engineered Exosomes Induces Nucleolar Stress to Suppress Cancer Progression.

Yu Gan, Qian Hao, Tao Han, Jing Tong, Qingya Yan, Hongguang Zhong, Bo Gao, Yanan Li, Zhisheng Xuan, Pengfei Li and 7 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Exosome-mediated siRNA delivery in cancer: Loading strategies, targeting approaches, and therapeutic outcomes.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
    Review
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  5. Article
  6. Research on exosomes in cancer multidrug resistance and clinical translation.Extracellular vesicles and circulating nucleic acids · 2026
    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

17 authors.

Yu GanFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, P. R. China.
Qian HaoFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, P. R. China.
Tao HanInstitutes of Health Central Plains, Xinxiang Key laboratory for Molecular Oncology, Xinxiang Medical University, Xinxiang, Henan, 453003, P. R. China.
Jing TongFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, P. R. China.
Qingya YanInstitutes of Health Central Plains, Xinxiang Key laboratory for Molecular Oncology, Xinxiang Medical University, Xinxiang, Henan, 453003, P. R. China.
Hongguang ZhongDepartment of Oncology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330006, P. R. China.
Bo GaoUmibio Co. Ltd., Shanghai, 201210, P. R. China.
Yanan LiUmibio Co. Ltd., Shanghai, 201210, P. R. China.
Zhisheng XuanUmibio Co. Ltd., Shanghai, 201210, P. R. China.
Pengfei LiLaboratory of Animal Center, Medical Experiment Center, Shaanxi University of Chinese Medicine, Xianyang, 712046, P. R. China.
Litong YaoDepartment of Breast Surgery, The First Hospital of China Medical University, Shenyang, Liaoning, 110001, P. R. China.
Yingying XuDepartment of Breast Surgery, The First Hospital of China Medical University, Shenyang, Liaoning, 110001, P. R. China.
Yi-Zhou JiangDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, P. R. China.
Zhi-Ming ShaoDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, P. R. China.
Jun DengDepartment of Oncology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330006, P. R. China.
Jiaxiang ChenDepartment of Physiology, School of Basic Medical Sciences, Jiangxi Medical College, Nanchang University, Nanchang, 330006, P. R. China.
Xiang ZhouFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, P. R. China.ORCID 0000-0002-1172-7948

Funding

Innovative Research Team of High-level Local University in ShanghaiJiangxi Province "Double Thousand Program" jxsq2023201108Key Projects of Jiangxi Province 20232ACB206044Major Discipline Academic and Technical Leaders Training Program of Jiangxi Province 20204BCJ22031National Natural Science Foundation of China 82002731National Natural Science Foundation of China 82060278National Natural Science Foundation of China 82072879National Natural Science Foundation of China 82171591National Natural Science Foundation of China 82172891National Natural Science Foundation of China 82173022National Natural Science Foundation of China 82202869National Natural Science Foundation of China 82260491National Natural Science Foundation of China 82273098Postdoctoral Fellowship Program of CPSF GZC20230494Postdoctoral grant 338937
6 · The paper itself

Abstract

Elevated ribosome biogenesis correlates with the rapid growth and progression of cancer. Targeted blockade of ribosome biogenesis induces nucleolar stress, which preferentially leads to the elimination of malignant cells. In this study, it is reported that the nucleolar protein BRIX1 is a critical regulator for the homeostasis between ribosome biogenesis and p53 activation. BRIX1 facilitated the processing of pre-rRNA by supporting the formation of the PeBoW complex. In addition, BRIX1 prevented p53 activation in response to nucleolar stress by impairing the interactions between MDM2 and the ribosomal proteins, RPL5, and RPL11, thereby triggering the resistance of cancer cells to chemotherapy. Conversely, depletion of BRIX1 induced nucleolar stress, which in turn activated p53 through RPL5 and RPL11, consequently inhibiting the growth of tumors. Moreover, engineered exosomes are developed, which are surface-decorated with iRGD, a tumor-homing peptide, and loaded with siRNAs specific to BRIX1, for the treatment of cancer. iRGD-Exo-siBRIX1 significantly suppressed the growth of colorectal cancer and enhanced the efficacy of 5-FU chemotherapy in vivo. Overall, the study uncovers that BRIX1 functions as an oncoprotein to promote rRNA synthesis and dampen p53 activity, and also implies that targeted inhibition of BRIX1 via engineered exosomes can be a potent approach for cancer therapy.

Indexed as

Disease ProgressionExosomesAnimalsCell Line, TumorCell NucleolusDisease Models, AnimalHumansMiceNeoplasmsNuclear ProteinsRibosomal ProteinsTumor Suppressor Protein p53Nuclear ProteinsRibosomal ProteinsTumor Suppressor Protein p53BRIX1engineered exosomesnucleolar stressp53ribosome biogenesistargeted therapy

Identifiers

PMID39475053
PMCPMC11653718

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.