Evidence map›Paper›PMID 27486982›Full record

ArticleOncotarget2016

Oncostatin M suppresses metastasis of lung adenocarcinoma by inhibiting SLUG expression through coordination of STATs and PIASs signalings.

Chih-Ming Pan, Mong-Lien Wang, Shih-Hwa Chiou, Hsiao-Yun Chen, Cheng-Wen Wu

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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 38 citations in OpenAlex.

  1. Trial
  2. Article
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  4. Mechanisms Underlying the Rarity of Skeletal Muscle Cancers.International journal of molecular sciences · 2024
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  8. Secretoglobin 3A2 protects lung from developing cigarette smoke-induced pulmonary emphysema.The international journal of biochemistry & cell biology · 2023
    Article
  9. Review
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  15. Article
  16. Review
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  18. Oncostatin M receptor, positively regulated by SP1, promotes gastric cancer growth and metastasis upon treatment with Oncostatin M.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2019
    Article
  19. Article
  20. Article
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 4 institutions in 1 country.

Chih-Ming PanInstitute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, Taiwan.
Mong-Lien WangInstitute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, Taiwan.
Shih-Hwa ChiouInstitute of Pharmacology, National Yang-Ming University, Taipei, Taiwan.
Hsiao-Yun ChenInstitute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan.
Cheng-Wen WuInstitute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, Taiwan.
National Yang Ming Chiao Tung University · TWInstitute of Molecular Biology, Academia Sinica · TWNational Yang Ming Chiao Tung University · TWNational Yang Ming University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oncostatin M (OSM) is linked with multiple biological responses including growth and differentiation. Previous reports showed inhibitory effects of OSM in tumor progression while others showed promoting effects. The dual role of OSM in the development of various cancers is still unclear. We previously described OSM-mediated SLUG suppression, leading to repressed metastasis of lung adenocarcinoma (LAC) cells. However, the underlying mechanism remains elusive. Here, we showed that OSM suppresses SLUG express in LAC cells through a STAT1-dependent transcriptional inhibition. Knockdown of STAT1 reversed the OSM-suppressed SLUG expression and rescued the OSM-mediated inhibition of cell proliferation, migration, and invasion in vitro, as well as pulmonary metastasis in vivo. STAT1 suppressed SLUG transcription through binding to its promoter region in response to OSM. Furthermore, PIAS4, a co-repressor of STAT, and HDAC1 were able to bind to STAT1 on SLUG promoter region, resulting in reduced H3K9 acetylation and suppressed SLUG expression upon OSM treatment. In contrast, PIAS3 bound to activated STAT3, another effector of OSM, in response to OSM and blocked the binding of STAT3 to SLUG promoter region, preventing STAT3-dependent activation of SLUG transcription. Our findings suggested that OSM suppresses SLUG expression and tumor metastasis of LAC through inducing the inhibitory effect of the STAT1-dependent pathway and suppressing the activating effect of STAT3-dependent signaling. These results can serve as a scientific basis for the potential therapeutic intervention of OSM in cancer cells.

Indexed as

AdenocarcinomaDown-RegulationGene Expression Regulation, NeoplasticHumansLung NeoplasmsNeoplasm MetastasisOncostatin MPoly-ADP-Ribose Binding ProteinsPromoter Regions, GeneticProtein Inhibitors of Activated STATSignal TransductionSnail Family Transcription FactorsSTAT1 Transcription FactorSTAT3 Transcription FactorTumor Cells, CulturedOncostatin MPIAS4 protein, humanPoly-ADP-Ribose Binding ProteinsProtein Inhibitors of Activated STATSNAI1 protein, humanSnail Family Transcription FactorsSTAT1 Transcription FactorSTAT3 protein, humanSTAT3 Transcription Factormetastasisoncostatin MPIAS4SLUGSTAT1

Identifiers

PMID27486982
PMCPMC5312391
OpenAlexW2489998297

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Registered trials

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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.