Exosome-Transferred STAT3 from Cancer-Associated Fibroblasts Expedites Thymic Carcinoma Malignant Progression and M2 Macrophage Polarization Through Transcriptionally Activating KLHL5.

Jianhu Chu, Dongbo Luo, Yang Wang, Yi Liu, Adili Shalai, Shiying Jin, Yunfei Gao

Abstract read

In one paragraph

Article in Applied biochemistry and biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it

0cells of the map it votes in

0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Jianhu ChuDepartment of Thoracic Surgery, Affiliated Tumor Hospital, Xinjiang Medical University, No.789 East Suzhou Street, Urumqi, 830011, Xinjiang, China.

Dongbo LuoDepartment of Thoracic Surgery, Affiliated Tumor Hospital, Xinjiang Medical University, No.789 East Suzhou Street, Urumqi, 830011, Xinjiang, China.

Yang WangDepartment of Thoracic Surgery, Affiliated Tumor Hospital, Xinjiang Medical University, No.789 East Suzhou Street, Urumqi, 830011, Xinjiang, China.

Yi LiuDepartment of Thoracic Surgery, Affiliated Tumor Hospital, Xinjiang Medical University, No.789 East Suzhou Street, Urumqi, 830011, Xinjiang, China.

Adili ShalaiDepartment of Thoracic Surgery, Affiliated Tumor Hospital, Xinjiang Medical University, No.789 East Suzhou Street, Urumqi, 830011, Xinjiang, China.

Shiying JinDepartment of Thoracic Surgery, Affiliated Tumor Hospital, Xinjiang Medical University, No.789 East Suzhou Street, Urumqi, 830011, Xinjiang, China.

Yunfei GaoDepartment of Thoracic Surgery, Affiliated Tumor Hospital, Xinjiang Medical University, No.789 East Suzhou Street, Urumqi, 830011, Xinjiang, China. gyf198436@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thymic carcinoma (THYM) is a mediastinal malignant tumor that seriously endangers human health. Cancer-associated fibroblasts (CAFs) are implicated in many cancers, but their role in THYM remains unclear. Western blot and reverse transcription-quantitative polymerase chain reaction were used to analyze expression levels. Exosomes were isolated and characterized by transmission electron microscopy and nanoparticle tracking analysis, and their uptake was assessed using PKH26 labeling. Cell functions were evaluated with cell counting kit-8, colony formation, and Transwell assays, while M2 macrophages were identified by flow cytometry for CD206. Bioinformatics databases analyzed gene correlations. The interaction between signal transducer and activator of transcription 3 (STAT3) and the kelch-like family member 5 (KLHL5) promoter was confirmed by chromatin immunoprecipitation and dual-luciferase reporter assay. Xenograft models were established to verify the effects of STAT3 in tumor growth, and protein expression in tissues was assessed by immunohistochemistry. Exosomes were successfully isolated from CAFs. STAT3 was up-regulated in CAF-derived exosomes compared to those from normal fibroblasts (NFs). Knockdown of STAT3 in CAF-derived exosomes repressed THYM cell viability, colony formation, migration, and invasion, as well as M2 macrophage polarization. STAT3 expression was positively correlated with KLHL5 and bound to the KLHL5 promoter. Furthermore, KLHL5 silence inhibited THYM cell malignant behaviors and M2 macrophage polarization, whereas KLHL5 overexpression attenuated the inhibitory effects of STAT3 knockdown. Similarly, silencing STAT3 in CAF-derived exosomes blocked tumor growth in vivo. CAF-derived exosomes transfer STAT3 to THYM cells, promoting THYM malignant progression and M2 macrophage polarization by transcriptionally activating KLHL5.

Indexed as

Cancer-Associated FibroblastsExosomesMacrophagesNeoplasm ProteinsSTAT3 Transcription FactorThymomaThymus NeoplasmsTranscriptional ActivationAnimalsCell Line, TumorDisease ProgressionHumansMiceNeoplasm ProteinsSTAT3 protein, humanSTAT3 Transcription FactorCancer-associated fibroblastsExosomesKelch-like family member 5Signal transducer and activator of transcription 3Thymic carcinoma

Identifiers

PMID41739296

DOI10.3390/ijms14011890

What Socratic holds

Textmetadata

Read underepoch 390

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.