Evidence map›Paper›PMID 40025525›Full record

ArticleJournal of experimental & clinical cancer research : CR2025

Exosome-transmitted LUCAT1 promotes stemness transformation and chemoresistance in bladder cancer by binding to IGF2BP2.

Yonghao Zhan, Zhenzhen Zhou, Zhaowei Zhu, Lianghao Zhang, Shuanbao Yu, Yuchen Liu, Xuepei Zhang

Abstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

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  20. Emerging technologies and current challenges in intratumoral microbiota research.Frontiers in cellular and infection microbiology · 2025
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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

7 authors.

Yonghao Zhan *Department of Urology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450003, China. yonghao_zhan@163.com.
Zhenzhen Zhou *Department of Urology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450003, China.
Zhaowei Zhu *Department of Urology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450003, China.
Lianghao ZhangDepartment of Urology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450003, China.
Shuanbao YuDepartment of Urology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450003, China.
Yuchen LiuShenzhen Institute of Translational Medicine, Health Science Center, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong, China. liuyuchenmdcg@163.com.
Xuepei ZhangDepartment of Urology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450003, China. zhangxuepei@263.net.

Funding

National Key Research and Development Program of China 2021YFA0911600
6 · The paper itself

Abstract

The chemotherapy resistance is an awkward challenge in management of bladder cancer (BC). Cancer organoid model is an effective preclinical tumor model that could faithfully represent clinical manifestations and simulate the biological processes of chemoresistance. Recent studies have revealed that cancer stem cells (CSCs) play a significant role in the development of chemoresistance in cancer. Exosomes act as essential intercellular messengers and participate in controlling the conversion of distinct cell characteristics, including chemoresistance. However, the role of exosome-transmitted lncRNAs in bladder cancer chemoresistance has rarely been reported. In this study, cancer organoid models were developed from urothelial carcinomas to explore the pathophysiology mechanism of BC chemoresistance, and RNA-seq was performed to screen for lncRNAs involved in chemoresistance of BC. We found chemotherapy enriches stem-like cells in BC, and significant upregulation of Lung Cancer Associated Transcript 1 (LUCAT1) occurs in chemotherapy-resistant organoids and correlated with chemotherapy response. Further experimental results demonstrated that LUCAT1 promotes chemoresistance in bladder cancer by enhancing the stemness phenotype of BC cells in vivo and in vitro. Moreover, exosomes derived from bladder cancer stem cells can enhance the stemness phenotype and chemoresistance of BC cells by delivering LUCAT1. Mechanistically, LUCAT1 could significantly enhance the mRNA stability of HMGA1 via binding to IGF2BP2 in an m6A-dependent manner. The study demonstrates an important role for exosome-transmitted LUCAT1 in chemoresistance and LUCAT1 has the potential to function as both a diagnostic biomarker and therapeutic target for BC.

Indexed as

Drug Resistance, NeoplasmExosomesNeoplastic Stem CellsRNA-Binding ProteinsRNA, Long NoncodingUrinary Bladder NeoplasmsAnimalsCell Line, TumorGene Expression Regulation, NeoplasticHumansMiceIGF2BP2 protein, humanRNA-Binding ProteinsRNA, Long NoncodingBladder cancerCancer stem cellChemoresistanceExosomeOrganoid

Identifiers

PMID40025525
PMCPMC11874664

What Socratic holds

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LicenceCC BY
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Registered trials

None linked

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 Socratic graph.