Evidence map›Paper›PMID 27276704›Full record

ArticleOncotarget2016

Modulation of macrophage polarization and lung cancer cell stemness by MUC1 and development of a related small-molecule inhibitor pterostilbene.

Wen-Chien Huang, Mei-Lin Chan, Ming-Jen Chen, Tung-Hu Tsai, Yu-Jen Chen

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
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  6. Article
  7. The multifaceted role of MUC1 in tumor therapy resistance.Clinical and experimental medicine · 2023
    Review
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  15. Article
  16. Article
  17. Cancer metastasis as a non-healing wound.British journal of cancer · 2021
    Review
  18. Review
  19. Article
  20. Comprehensive analysis of the mechanism and treatment significance of Mucins in lung cancer.Journal of experimental & clinical cancer research : CR · 2020
    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 3 institutions in 1 country.

Wen-Chien HuangMacKay Medical College, Taipei, Taiwan.
Mei-Lin ChanMacKay Medical College, Taipei, Taiwan.
Ming-Jen ChenInstitute of Traditional Medicine, School of Medicine, National Yang Ming University, Taipei, Taiwan.
Tung-Hu TsaiMacKay Medical College, Taipei, Taiwan.
Yu-Jen ChenMacKay Medical College, Taipei, Taiwan.
Mackay Memorial Hospital · TWMackay Medical College · TWNational Yang Ming Chiao Tung University · TW

Funding

Reward Learning in Late-Life Suicidal BehaviorR01MH100095 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Alexandre Y. Dombrovski · 2014 to 2026
$6.8M
NIMH NIH HHS R01 MH100095
6 · The paper itself

Abstract

Tumor-associated macrophages (TAMs) polarized to the M2 phenotype play key roles in tumor progression in different cancer types, including lung cancer. MUC1 expression in various types of cancer is an indicator of poorer prognosis. Elevated MUC1 expression has been reported in inflammatory lung macrophages and is associated with lung cancer development. Here, we investigated the role of M2-polarized TAMs (M2-TAMs) in the generation of lung cancer stem cells (LCSCs) and tested pterostilbene, a small-molecule agent that modulates MUC1 expression in lung cancer cells, with the goal of subverting the microenvironment toward a favorable anti-tumor impact. We found that MUC1 was overexpressed in lung cancer patients, which was associated with poor survival rates. M2-TAMs and cancer cell lines were co-cultured in an experimental tumor microenvironment model. The expression levels of MUC1 and cancer stemness genes significantly increased in lung cancer cells in the presence of the M2-TAM cells. Intriguingly, pterostilbene dose-dependently suppressed self-renewal ability in M2-TAMs-co-cultured lung cancer cells, and this suppression was accompanied by downregulation of MUC1, NF-κB, CD133, β-catenin, and Sox2 expression. Moreover, MUC1-silenced M2-TAMs exhibited a significantly lower ability to promote LCSC generation and decreased levels of NF-κB, CD133, and Sox2. The results suggest that MUC1 plays an important role in TAM-induced LCSC progression. Pterostilbene may have therapeutic potential for modulating the unfavorable effects of TAMs in lung cancer progression.

Indexed as

A549 CellsAC133 AntigenCarcinoma, Non-Small-Cell LungCell Line, TumorCell SeparationCoculture TechniquesDisease ProgressionFlow CytometryGene Expression ProfilingGene SilencingHumansImmune SystemInflammationLung NeoplasmsMacrophagesMucin-1AC133 AntigenMUC1 protein, humanMucin-1PROM1 protein, humanpterostilbeneStilbenesImmune responseImmunityImmunology and Microbiology Sectionlung cancer stem cells (CSCs)M2 polarizationMUC1pterostilbenetumor-associated macrophages (TAMs)

Identifiers

PMID27276704
PMCPMC5129938
OpenAlexW2404685178

What OpenQuestion holds

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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.