Evidence map›Paper›PMID 40248740›Full record

ArticleTranslational lung cancer research2025

Circulating lung cancer exosomes damage the niche of intestinal stem cells.

Ke Wang, Lu Xu, Jianhua Feng, Shubin Wang, Xi Wang, Junyi Zou, Zhenni Xu, Lingxiao Huang, Wenjun Jiang, Jin Zhou and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Translational lung cancer research, 2025. 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. Review
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

12 authors.

Ke Wang *Department of Oncology, Sichuan Cancer Hospital & Institute, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Lu Xu *Radiation Oncology Key Laboratory of Sichuan Province, Department of Experimental Research, Sichuan Cancer Hospital & Institute, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Jianhua Feng *Department of Oncology, Sichuan Cancer Hospital & Institute, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Shubin Wang *Department of Oncology, Sichuan Cancer Hospital & Institute, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Xi WangRadiation Oncology Key Laboratory of Sichuan Province, Department of Experimental Research, Sichuan Cancer Hospital & Institute, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Junyi ZouDepartment of Oncology, Sichuan Cancer Hospital & Institute, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Zhenni XuRadiation Oncology Key Laboratory of Sichuan Province, Department of Experimental Research, Sichuan Cancer Hospital & Institute, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Lingxiao HuangRadiation Oncology Key Laboratory of Sichuan Province, Department of Experimental Research, Sichuan Cancer Hospital & Institute, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Wenjun JiangRadiation Oncology Key Laboratory of Sichuan Province, Department of Experimental Research, Sichuan Cancer Hospital & Institute, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Jin ZhouDepartment of Oncology, Sichuan Cancer Hospital & Institute, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Xudan LeiRadiation Oncology Key Laboratory of Sichuan Province, Department of Experimental Research, Sichuan Cancer Hospital & Institute, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Dengqun LiuRadiation Oncology Key Laboratory of Sichuan Province, Department of Experimental Research, Sichuan Cancer Hospital & Institute, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Cancer-associated weight loss occurs frequently in patients with advanced lung cancer. Many studies have demonstrated that tumor-derived exosomes could mediate the interplay between tumor cells and distal organs. In this study, we explored the interaction between lung cancer cell-derived exosomes (LCCDEs) and the niche of intestinal stem cells (ISCs). Methods: Lewis lung carcinoma-1 (LLC1)-conditional medium (LLC1-CM), N,N'-Bis[5-(2,3-dihydro-1H-indol-1-yl)pentyl]-1,6-hexanediamine (GW4869)-conditional medium (GW4869-CM), LCCDEs and phosphate-buffered saline (PBS) were used to treat 6- to 8-week-old healthy male C57BL/6J mice (18-22 g) and B6.129P2-Lgr5 Results: LLC1-CM damaged the small intestines and small intestinal organoids. The inhibition of exosomes by GW4869 partially alleviated these effects. Purified LCCDEs altered the structure of the intestines, changed the proliferation and differentiation of ISCs and inhibited the growth of enteroids. In addition, PKH26-labeled LCCDEs entered the cytoplasm of IECs and Paneth cells and changed the messenger ribonucleic acid (mRNA) expression of many genes, including stem cell marker genes, growth factor genes, and epithelial marker genes. Mechanistically, LCCDEs decreased mTORC1 activity in Paneth cells and inhibited p-ERK1/2 signaling in ISCs. Conclusions: We demonstrated that circulating exosomes derived from lung cancer could impair ISCs and alter their niche in mice, which further explained the interaction between lung cancer and the gastrointestinal tract. This study proposes a promising and novel therapy to overcome weight loss in patients by decreasing LCCDEs secretion and blocking their binding to the intestine, which might be a feasible therapeutic approach in future clinical practice.

Indexed as

exosomeintestinal stem cell (ISC)Lgr5Lung cancermicroenvironment

Identifiers

PMID40248740
PMCPMC12000945

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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.