Evidence map›Paper›PMID 37005676›Full record

ArticleJournal of translational medicine2023

LncRNA H19-rich extracellular vesicles derived from gastric cancer stem cells facilitate tumorigenicity and metastasis via mediating intratumor communication network.

Hongying Zhao, Rongke Jiang, Chunmei Zhang, Zhijing Feng, Xue Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  3. Article
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  6. Gelsolin's Protective Role in MASH through F-Actin Regulation and P53 Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. FAM117A and PIGU regulate the trilogy of gastric carcinogenesis.Computational and structural biotechnology journal · 2025
    Article
  12. Review
  13. Review
  14. Altered Levels ofIn vivo (Athens, Greece)
    Article
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

5 authors at 2 institutions in 1 country.

Hongying ZhaoDepartment of Oncology, Xuzhou City Cancer Hospital, Xuzhou Third People's Hospital, Xuzhou Hospital Affiliated to Jiangsu University, No. 131 Huancheng Road, Gulou District, Xuzhou, 221000, People's Republic of China. zhaohy8777@163.com.
Rongke JiangDepartment of Oncology, Xuzhou City Cancer Hospital, Xuzhou Third People's Hospital, Xuzhou Hospital Affiliated to Jiangsu University, No. 131 Huancheng Road, Gulou District, Xuzhou, 221000, People's Republic of China.
Chunmei ZhangJiangsu University, Zhenjiang, 212013, People's Republic of China.
Zhijing FengJiangsu University, Zhenjiang, 212013, People's Republic of China.
Xue WangDepartment of Oncology, Xuzhou City Cancer Hospital, Xuzhou Third People's Hospital, Xuzhou Hospital Affiliated to Jiangsu University, No. 131 Huancheng Road, Gulou District, Xuzhou, 221000, People's Republic of China.
Jiangsu University · CNXuzhou Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundExtracellular vesicles (EVs) transport biologically active molecules, and represent a recently identified way of intercellular communication. Recent evidence has also reported that EVs shed by cancer stem cells (CSCs) make a significant contribution to carcinogenesis and metastasis. Here, this study aims to explore the possible molecular mechanism of CSCs-EVs in gastric cancer (GC) by mediating intratumor communication network.

methodsCSCs and non-stem cancer cells (NSCCs) were sorted from GC cells, and EVs were isolated from CSCs. H19 was knocked down in CSCs, and CSCs-EVs or CSCs-EVs containing shRNA-H19 (CSCs-EVs-sh-H19) were co-cultured with NSCCs, followed by evaluation of the malignant behaviors and stemness of NSCCs. Mouse models of GC were established and injected with CSCs-EVs from sh-H19-treated NSCCs in vivo.

resultsCSCs had notable self-renewal and tumorigenic capacity compared with NSCCs. CSCs promoted the malignant behaviors of NSCCs and expression of stemness marker proteins through secretion of EVs. Inhibited secretion of CSCs-EVs curtailed the tumorigenicity and metastasis of NSCCs in vivo. H19 could be delivered by CSCs-EVs into NSCCs. H19 promoted the malignant behaviors of NSCCs and stemness marker protein expression in vitro along with tumorigenicity and liver metastasis in vivo, which was mechanistically associated with activation of the YAP/CDX2 signaling axis.

conclusionTaken together, the present study points to the importance of a novel regulatory axis H19/YAP/CDX2 in carcinogenic and metastatic potential of CSCs-EVs in GC, which may be potential targets for anticancer therapy.

Indexed as

Extracellular VesiclesRNA, Long NoncodingStomach NeoplasmsAnimalsCarcinogenesisCell Line, TumorMiceNeoplastic Stem CellsProteinsSignal TransductionProteinsRNA, Long NoncodingCancer stem cellsCDX2Extracellular vesiclesGastric cancerIntratumor communication networkLncRNA H19YAP

Identifiers

PMID37005676
PMCPMC10067256
OpenAlexW4362521510

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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 OpenQuestion graph.