Evidence map›Paper›PMID 31761621›Full record

ArticleEBioMedicine2019

Aberrant expression of embryonic mesendoderm factor MESP1 promotes tumorigenesis.

Neha Tandon, Kristina Goller, Fan Wang, Benjamin Soibam, Mihai Gagea, Abhinav K Jain, Robert J Schwartz, Yu Liu

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.3field-weighted citation impact, top 40% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

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  8. High levels ofTranslational cancer research · 2020
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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

8 authors at 4 institutions in 2 countries.

Neha TandonDepartment of Biology and Biochemistry, University of Houston, Houston, TX, United States.
Kristina GollerDepartment of Biology and Biochemistry, University of Houston, Houston, TX, United States.
Fan WangDepartment of Biology and Biochemistry, University of Houston, Houston, TX, United States; Department of Oncology, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.
Benjamin SoibamComputer Science and Engineering Technology, University of Houston-Downtown, Houston, TX, United States.
Mihai GageaDepartment of Veterinary Medicine and Surgery, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Abhinav K JainCenter for Cancer Epigenetics, Department of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Robert J SchwartzDepartment of Biology and Biochemistry, University of Houston, Houston, TX, United States.
Yu LiuDepartment of Biology and Biochemistry, University of Houston, Houston, TX, United States. Electronic address: yliu54@uh.edu.
University of Houston · USThe University of Texas MD Anderson Cancer Center · USFirst Affiliated Hospital of Xi'an Jiaotong University · CNUniversity of Houston - Downtown · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMesoderm Posterior 1 (MESP1) belongs to the family of basic helix-loop-helix transcription factors. It is a master regulator of mesendoderm development, leading to formation of organs such as heart and lung. However, its role in adult pathophysiology remains unknown. Here, we report for the first time a previously-unknown association of MESP1 with non-small cell lung cancer (NSCLC).

methodsMESP1 mRNA and protein levels were measured in NSCLC-derived cells by qPCR and immunoblotting respectively. Colony formation assay, colorimetric cell proliferation assay and soft agar colony formation assays were used to assess the effects of MESP1 knockdown and overexpression in vitro. RNA-sequencing and chromatin immunoprecipitation (ChIP)-qPCR were used to determine direct target genes of MESP1. Subcutaneous injection of MESP1-depleted NSCLC cells in immuno-compromised mice was done to study the effects of MESP1 mediated tumor formation in vivo.

findingsWe found that MESP1 expression correlates with poor prognosis in NSCLC patients, and is critical for proliferation and survival of NSCLC-derived cells, thus implicating MESP1 as a lung cancer oncogene. Ectopic MESP1 expression cooperates with loss of tumor suppressor ARF to transform murine fibroblasts. Xenografts from MESP1-depleted cells showed decreased tumor growth in vivo. Global transcriptome analysis revealed a MESP1 DNA-binding-dependent gene signature associated with various hallmarks of cancer, suggesting that transcription activity of MESP1 is most likely responsible for its oncogenic abilities.

interpretationOur study demonstrates MESP1 as a previously-unknown lineage-survival oncogene in NSCLC which may serve as a potential prognostic marker and therapeutic target for lung cancer in the future.

Indexed as

Gene Expression RegulationAnimalsBasic Helix-Loop-Helix ProteinsCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationCell Transformation, NeoplasticComputational BiologyDisease Models, AnimalGene Expression ProfilingHeterograftsHumansLung NeoplasmsMiceBasic Helix-Loop-Helix ProteinsMESP1 protein, humanMesp1 protein, mouseARFLineage-survival oncogeneLung cancerMesp1

Identifiers

PMID31761621
PMCPMC6921370
OpenAlexW2990735016

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.