Evidence map›Paper›PMID 38205211›Full record

ArticleTranslational lung cancer research2023

Exosomal ITGB6 from dormant lung adenocarcinoma cells activates cancer-associated fibroblasts by KLF10 positive feedback loop and the TGF-β pathway.

Xiang Feng, Xianling Liu, Juanjuan Xiang, Jiaqi Xu, Na Yin, Lujuan Wang, Chaoyuan Liu, Yuyao Liu, Tiantian Zhao, Zengyi Zhao and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Translational lung cancer research, 2023. 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
2.6field-weighted citation impact, top 10% of its field
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, 17 citations in OpenAlex.

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  11. [Mechanisms of Exosomes in Lung Cancer Bone Metastasis and Related Clinical Advances].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 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

11 authors at 2 institutions in 1 country.

Xiang FengDepartment of Oncology, The Second Xiangya Hospital of Central South University, Changsha, China.
Xianling LiuDepartment of Oncology, The Second Xiangya Hospital of Central South University, Changsha, China.
Juanjuan XiangCancer Research Institute, School of Basic Medical Science, Central South University, Changsha, China.
Jiaqi XuCancer Research Institute, School of Basic Medical Science, Central South University, Changsha, China.
Na YinCancer Research Institute, School of Basic Medical Science, Central South University, Changsha, China.
Lujuan WangCancer Research Institute, School of Basic Medical Science, Central South University, Changsha, China.
Chaoyuan LiuDepartment of Oncology, The Second Xiangya Hospital of Central South University, Changsha, China.
Yuyao LiuDepartment of Oncology, The Second Xiangya Hospital of Central South University, Changsha, China.
Tiantian ZhaoDepartment of Oncology, The Second Xiangya Hospital of Central South University, Changsha, China.
Zengyi ZhaoDepartment of Oncology, The Second Xiangya Hospital of Central South University, Changsha, China.
Yawen GaoDepartment of Oncology, The Second Xiangya Hospital of Central South University, Changsha, China.
Central South University · CNSecond Xiangya Hospital of Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Dormant cancer cells are commonly known to play a pivotal role in cancer recurrence and metastasis. However, the mechanism of tumor dormancy and recurrence remains largely unknown. This study aimed to investigate the mechanism by which exosomes derived from dormant lung adenocarcinoma (LUAD) cells activate cancer-associated fibroblasts (CAFs) to reconstruct the extracellular matrix (ECM), providing a novel idea for decoding the mechanism of tumor dormancy. Methods: In this study, high-dose cisplatin was used to induce the dormant LUAD cells. Exosomes were extracted from the culture supernatant of normal and dormant cancer cells. The effects of selected exosomal proteins on the fibroblasts were evaluated. RNA-seq for fibroblasts and exosomal proteomics for normal and dormant cancer cells were used to identify and verify the mechanism of activating fibroblasts. Results: We demonstrated that exosomes derived from dormant A549 cells could be taken by fibroblasts. Exosomal ITGB6 transferred into fibroblasts induced the activation of CAFs by activating the KLF10 positive feedback loop and transforming growth factor β (TGF-β) pathway. High ITGB6 expression was associated with activation of the TGF-β pathway and ECM remodeling. Conclusions: In all, we demonstrated that CAFs were activated by exosomes from dormant lung cancer cells and reconstruct ECM. ITGB6 may be a critical molecule for activating the TGF-β pathway and remodeling ECM.

Indexed as

cancer-associated fibroblasts (CAFs)dormancyexosomesLung cancer

Identifiers

PMID38205211
PMCPMC10775012
OpenAlexW4390238032

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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 OpenQuestion graph.