Evidence map›Paper›PMID 26515338›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

Secretome of human bone marrow mesenchymal stem cells: an emerging player in lung cancer progression and mechanisms of translation initiation.

Oshrat Attar-Schneider, Victoria Zismanov, Liat Drucker, Maya Gottfried

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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 46 citations in OpenAlex.

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  10. Tumor-Derived Exosomal eIF4E as a Biomarker for Survival Prediction in Patients with Non-Small Cell Lung Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2020
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  14. Advanced pharmaceutical bulletin · 2019
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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

4 authors at 2 institutions in 1 country.

Oshrat Attar-SchneiderLung Cancer Research, Meir Medical Center, Kfar Saba, 44281, Israel. oshrat.attar@clalit.org.il.
Victoria ZismanovLung Cancer Research, Meir Medical Center, Kfar Saba, 44281, Israel.
Liat DruckerOncogenetic Laboratories, Meir Medical Center, Kfar Saba, 44281, Israel.
Maya GottfriedLung Cancer Research, Meir Medical Center, Kfar Saba, 44281, Israel.
Meir Medical Center · ILTel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC) remains the most common cause of cancer-related death worldwide. Patients presenting with advanced-stage NSCLC have poor prognosis, while metastatic spread accounts for >70 % of patient's deaths. The major advances in the treatment of lung cancer have brought only minor improvements in survival; therefore, novel strategic treatment approaches are urgently needed. Accumulating data allocate a central role for the cancer microenvironment including mesenchymal stem cells (MSCs) in acquisition of drug resistance and disease relapse. Furthermore, studies indicate that translation initiation factors are over expressed in NSCLC and negatively impact its prognosis. Importantly, translation initiation is highly modulated by microenvironmental cues. Therefore, we decided to examine the effect of bone marrow MSCs (BM-MSCs) from normal donors on NSCLC cell lines with special emphasis on translation initiation mechanism in the crosstalk. We cultured NSCLC cell lines with BM-MSC conditioned media (i.e., secretome) and showed deleterious effects on the cells' proliferation, viability, death, and migration. We also demonstrated reduced levels of translation initiation factors implicated in cancer progression [eukaryotic translation initiation factor 4E (eIF4E) and eukaryotic translation initiation factor 4GI (eIF4GI)], their targets, and regulators. Finally, we outlined a mechanism by which BM-MSCs' secretome affected NSCLC's mitogen-activated protein kinase (MAPK) signaling pathway, downregulated the cell migration, and diminished translation initiation factors' levels. Taken together, our study demonstrates that there is direct dialogue between the BM-MSCs' secretome and NSCLC cells that manipulates translation initiation and critically affects cell fate. We suggest that therapeutic approach that will sabotage this dialogue, especially in the BM microenvironment, may diminish lung cancer metastatic spread and morbidity and improve the patient's life quality.

Indexed as

Peptide Chain Initiation, TranslationalAgedCarcinoma, Non-Small-Cell LungCell MovementCell ProliferationCell SurvivalDisease ProgressionEukaryotic Initiation Factor-4GFemaleHumansLung NeoplasmsMaleMesenchymal Stem CellsMitogen-Activated Protein KinasesNeoplastic Stem CellsNucleocytoplasmic Transport ProteinsEIF4ENIF1 protein, humanEIF4G1 protein, humanEukaryotic Initiation Factor-4GMitogen-Activated Protein KinasesNucleocytoplasmic Transport ProteinsProteomeeIF4E/eIF4GIHuman mesenchymal stem cellsMigrationNSCLCTranslation initiation

Identifiers

PMID26515338
OpenAlexW1925324900

What OpenQuestion 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 OpenQuestion graph.