Evidence map›Paper›PMID 34244494›Full record

Observational studyNature communications2021

Extracellular matrix protein-1 secretory isoform promotes ovarian cancer through increasing alternative mRNA splicing and stemness.

Huijing Yin, Jingshu Wang, Hui Li, Yinjue Yu, Xiaoling Wang, Lili Lu, Cuiting Lv, Bin Chang, Wei Jin, Wenwen Guo and 2 more

Open access · goldAbstract readObservational Study
In one paragraph

Observational study in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.2field-weighted citation impact, top 4% 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

46 citing papers in PubMed, 74 citations in OpenAlex.

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  17. Alternative splicing in ovarian cancer.Cell communication and signaling : CCS · 2024
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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

12 authors at 4 institutions in 1 country.

Huijing Yin *Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, China.
Jingshu Wang *Central Laboratory, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Hui Li *Central Laboratory, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Yinjue Yu *Central Laboratory, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Xiaoling WangCenter for Reproductive Medicine, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Lili LuCancer Institute, Fudan University Shanghai Cancer Center, Shanghai, China.
Cuiting LvCentral Laboratory, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Bin ChangDepartment of Oncology, Shanghai Medical School, Fudan University, Shanghai, China.
Wei JinDepartment of Pathology, The People's Hospital of Guangxi Zhuang Autonomous Region, Guangxi, China.
Wenwen GuoDepartment of Oncology, Shanghai Medical School, Fudan University, Shanghai, China.
Chunxia RenCenter for Reproductive Medicine, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China. renchunxia2018@shutcm.edu.cn.ORCID 0000-0002-2950-4419
Gong YangCancer Institute, Fudan University Shanghai Cancer Center, Shanghai, China. yanggong@fudan.edu.cn.ORCID 0000-0002-5137-4104
Shanghai Medical College of Fudan University · CNFudan University · CNShanghai University of Traditional Chinese Medicine · CNThe People's Hospital of Guangxi Zhuang Autonomous Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extracellular matrix protein-1 (ECM1) promotes tumorigenesis in multiple organs but the mechanisms associated to ECM1 isoform subtypes have yet to be clarified. We report in this study that the secretory ECM1a isoform induces tumorigenesis through the GPR motif binding to integrin αXβ2 and the activation of AKT/FAK/Rho/cytoskeleton signaling. The ATP binding cassette subfamily G member 1 (ABCG1) transduces the ECM1a-integrin αXβ2 interactive signaling to facilitate the phosphorylation of AKT/FAK/Rho/cytoskeletal molecules and to confer cancer cell cisplatin resistance through up-regulation of the CD326-mediated cell stemness. On the contrary, the non-secretory ECM1b isoform binds myosin and blocks its phosphorylation, impairing cytoskeleton-mediated signaling and tumorigenesis. Moreover, ECM1a induces the expression of the heterogeneous nuclear ribonucleoprotein L like (hnRNPLL) protein to favor the alternative mRNA splicing generating ECM1a. ECM1a, αXβ2, ABCG1 and hnRNPLL higher expression associates with poor survival, while ECM1b higher expression associates with good survival. These results highlight ECM1a, integrin αXβ2, hnRNPLL and ABCG1 as potential targets for treating cancers associated with ECM1-activated signaling.

Indexed as

Alternative SplicingAnimalsATP Binding Cassette Transporter, Subfamily G, Member 1Carcinoma, Ovarian EpithelialCell Line, TumorChemotherapy, AdjuvantCisplatinDisease-Free SurvivalDrug Resistance, NeoplasmExtracellular Matrix ProteinsFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticHeterogeneous-Nuclear RibonucleoproteinsHumansIntegrin alphaXbeta2ABCG1 protein, humanATP Binding Cassette Transporter, Subfamily G, Member 1CisplatinECM1 protein, humanExtracellular Matrix ProteinsHeterogeneous-Nuclear RibonucleoproteinsHNRNPLL protein, humanIntegrin alphaXbeta2Protein Isoforms

Identifiers

PMID34244494
PMCPMC8270969
OpenAlexW3182698864

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.