Evidence map›Paper›PMID 37941042›Full record

ArticleCell & bioscience2023

Musashi-2 in cancer-associated fibroblasts promotes non-small cell lung cancer metastasis through paracrine IL-6-driven epithelial-mesenchymal transition.

Parinya Samart, Gayathri Heenatigala Palliyage, Surapol Issaragrisil, Sudjit Luanpitpong, Yon Rojanasakul

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
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 2 countries.

Parinya SamartDepartment of Pharmaceutical Sciences, West Virginia University, Morgantown, WV, 26506, USA.
Gayathri Heenatigala PalliyageDepartment of Pharmaceutical Sciences, West Virginia University, Morgantown, WV, 26506, USA.
Surapol IssaragrisilSiriraj Center of Excellence for Stem Cell Research, Faculty of Medicine Siriraj Hospital, Mahidol University, 2 Siriraj Hospital, Bangkoknoi, Bangkok, 10700, Thailand.
Sudjit LuanpitpongSiriraj Center of Excellence for Stem Cell Research, Faculty of Medicine Siriraj Hospital, Mahidol University, 2 Siriraj Hospital, Bangkoknoi, Bangkok, 10700, Thailand. suidjit@gmail.com.ORCID http://orcid.org/0000-0002-1639-4935
Yon RojanasakulDepartment of Pharmaceutical Sciences, West Virginia University, Morgantown, WV, 26506, USA. yrojan@hsc.wvu.edu.
West Virginia University · USSiriraj Hospital · TH

Funding

Nanoparticle Fibrogenicity and Fibroblast Stem-Like CellsR01EB018857 · NIBIB · WEST VIRGINIA UNIVERSITY · PI ROJANASAKUL, YON · 2016 to 2019
$1.3M
NIBIB NIH HHS R01 EB018857NIH HHS R01-EB018857NIH HHS R01-ES02296
6 · The paper itself

Abstract

backgroundLung cancer, the most common cause of cancer-related mortality worldwide, is predominantly associated with advanced/metastatic disease. The interaction between tumor cells and cancer-associated fibroblasts (CAFs) in tumor microenvironment is known to be essential for regulating tumor progression and metastasis, but the underlying mechanisms, particularly the role of RNA-binding protein Musashi-2 (MSI2) in CAFs in promoting non-small cell lung cancer (NSCLC) invasiveness and metastatic spread, remain obscure.

methodsGenomic and proteomic database analyses were performed to evaluate the potential clinical significance of MSI2 in NSCLC tumor and stromal clinical specimens. Molecular approaches were used to modify MSI2 in CAFs and determine its functional role in NSCLC cell motility in vitro using 2D and 3D models, and in metastasis in a xenograft mouse model using live-cell imaging.

resultsMSI2, both gene and protein, is upregulated in NSCLC tissues and is associated with poor prognosis and high metastatic risk in patients. Interestingly, MSI2 is also upregulated in NSCLC stroma and activated fibroblasts, including CAFs. Depletion of MSI2 in CAFs by CRISPR-Cas9 strongly inhibits NSCLC cell migration and invasion in vitro, and attenuates local and distant metastatic spread of NSCLC cells in vivo. The crosstalk between CAFs and NSCLC cells occurs via paracrine signaling, which is regulated by MSI2 in CAFs via IL-6. The secreted IL-6 promotes epithelial-mesenchymal transition in NSCLC cells, which drives metastasis.

conclusionOur findings reveal for the first time that MSI2 in CAFs is important in CAF-mediated NSCLC cell invasiveness and metastasis via IL-6 paracrine signaling. Therefore, targeting the MSI2/IL-6 axis in CAFs could be effective in combating NSCLC metastasis.

Indexed as

Cancer-associated fibroblastEpithelial-mesenchymal transitionIL-6MetastasisMusashi-2Non-small cell lung cancerTumor microenvironment

Identifiers

PMID37941042
PMCPMC10631049
OpenAlexW4388496288

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.