Evidence map›Paper›PMID 32300102›Full record

ArticleCell death & disease2020

MSC-induced lncRNA HCP5 drove fatty acid oxidation through miR-3619-5p/AMPK/PGC1α/CEBPB axis to promote stemness and chemo-resistance of gastric cancer.

Honglei Wu, Bin Liu, Zhaosheng Chen, Guangchun Li, Zhen Zhang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed, 1 pooled it
16.0field-weighted citation impact, top 1% 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

156 citing papers in PubMed, 1 synthesis or guideline pooled it, 286 citations in OpenAlex.

  1. Pooled it
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  8. Journal of hepatocellular carcinoma · 2026
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96 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Honglei WuDepartment of Gastroenterology, the Second Hospital of Shandong University, No.247 Beiyuan Street, 250033, Jinan, Shandong, China.
Bin LiuDepartment of Gastroenterology, the Second Hospital of Shandong University, No.247 Beiyuan Street, 250033, Jinan, Shandong, China. binliu.2009@163.com.
Zhaosheng ChenDepartment of Gastroenterology, the Second Hospital of Shandong University, No.247 Beiyuan Street, 250033, Jinan, Shandong, China.
Guangchun LiDepartment of Gastroenterology, the Second Hospital of Shandong University, No.247 Beiyuan Street, 250033, Jinan, Shandong, China.
Zhen ZhangDepartment of Gastroenterology, the Second Hospital of Shandong University, No.247 Beiyuan Street, 250033, Jinan, Shandong, China.
Second Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemotherapy is the first-tier treatment regime for gastric cancer (GC) patients at advance stages. Mesenchymal stem cell (MSC) cam affect drug-resistance of GC cells in tumor microenvironment, but the detailed mechanism remains poorly understood. Present study aimed to investigate the regulation of MSC-induced long non-coding RNA (lncRNA) in GC. Dysregulated lncRNAs in GC were analyzed based on GEO data. Stemness and drug-resistance of GC cells were detected by sphere formation, colony formation, CCK-8, and flow cytometry analyses. MicroRNA (miRNA)-related pathways were analyzed by online KEGG analysis tool DAVID6.8. Molecular interactions were determined by luciferase reporter assay, pulldown, RNA immunoprecipitation (RIP), chromatin immunoprecipitation (ChIP), and co-immunoprecipitation (CoIP). Results revealed that MSC co-culture improved stemness and drug-resistance of GC cells. LncRNA histocompatibility leukocyte antigen complex P5 (HCP5) was induced in GC cells by MSC co-culture, contributing to stemness and drug-resistance. Mechanistically, HCP5 sequestered miR-3619-5p and upregulated PPARG coactivator 1 alpha (PPARGC1A), increasing transcription complex Peroxisome proliferator activated receptor (PPAR) coactivator-1α (PGC1α)/CEBPB and transcriptionally inducing carnitine palmitoyltransferase 1 (CPT1), which prompted the fatty acid oxidation (FAO) in GC cells. In conclusion, MSC-induced lncRNA HCP5 drove FAO through miR-3619-5p/AMPK/PGC1α/CEBPB axis to promote stemness and chemo-resistance of GC, indicating that targeting HCP5 was a novel approach to enhancing the efficacy of chemotherapy in GC.

Indexed as

3-Hydroxyacyl CoA DehydrogenasesAcetyl-CoA C-AcyltransferaseAMP-Activated Protein KinasesAnimalsCarbon-Carbon Double Bond IsomerasesDrug Resistance, NeoplasmEnoyl-CoA HydrataseFatty AcidsHumansMiceMice, NudeNeoplastic Stem CellsOxidation-ReductionRacemases and EpimerasesRNA, Long NoncodingStomach Neoplasms3-Hydroxyacyl CoA DehydrogenasesAcetyl-CoA C-AcyltransferaseAMP-Activated Protein KinasesCarbon-Carbon Double Bond IsomerasesEnoyl-CoA Hydratasefatty acid oxidation complexFatty AcidsHCP5 long noncoding RNA, humanRacemases and EpimerasesRNA, Long Noncoding

Identifiers

PMID32300102
PMCPMC7162922
OpenAlexW3016678766

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.