Evidence map›Paper›PMID 26586569›Full record

ArticleCell death and differentiation2016

Downregulation of COMMD1 by miR-205 promotes a positive feedback loop for amplifying inflammatory- and stemness-associated properties of cancer cells.

D-W Yeh, Y-S Chen, C-Y Lai, Y-L Liu, C-H Lu, J-F Lo, L Chen, L-C Hsu, Y Luo, R Xiang and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 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
1.3field-weighted citation impact, top 21% 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, 51 citations in OpenAlex.

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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

11 authors at 7 institutions in 2 countries.

D-W YehImmunology Research Center, National Health Research Institutes, Miaoli, Taiwan.
Y-S ChenInstitute of Oral Biology, National Yang-Ming University, Taipei, Taiwan.
C-Y LaiImmunology Research Center, National Health Research Institutes, Miaoli, Taiwan.
Y-L LiuImmunology Research Center, National Health Research Institutes, Miaoli, Taiwan.
C-H LuImmunology Research Center, National Health Research Institutes, Miaoli, Taiwan.
J-F LoInstitute of Oral Biology, National Yang-Ming University, Taipei, Taiwan.
L ChenInstitute of Molecular Medicine, National Tsing-Hua University, Hsinchu, Taiwan.
L-C HsuInstitute of Molecular Medicine, National Taiwan University, Taipei, Taiwan.
Y LuoDepartment of Immunology, Institute of Basic Medical Science, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China.
R XiangSchool of Medicine, University of Nankai, Tianjin, PR China.
T-H ChuangImmunology Research Center, National Health Research Institutes, Miaoli, Taiwan.
National Health Research Institutes · TWChinese Academy of Medical Sciences & Peking Union Medical College · CNNankai University · CNNational Taiwan University · TWNational Tsing Hua University · TWNational Yang Ming Chiao Tung University · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sustained activation of nuclear factor-κB (NF-κB) in cancer cells has been shown to promote inflammation, expansion of cancer stem cell (CSC) population, and tumor development. In contrast, recent studies reveal that CSCs exhibit increased inflammation due to constitutive NF-κB activation; however, the underlying molecular mechanism remains unclear. In the present study, the analysis of microarray data revealed upregulation of NF-κB-regulated pro-inflammatory genes and downregulation of copper metabolism MURR1 domain-containing 1 (COMMD1) during the enrichment for stemness in SAS head and neck squamous-cell carcinoma (HNSCC) cells. The 3'-UTR of COMMD1 mRNA contains microRNA (miR)-205 target site. Parallel studies with HNSCC and NSCLC cells indicated that miR-205 is upregulated upon NF-κB activation and suppresses COMMD1 expression in stemness-enriched cancer cells. COMMD1 negatively regulates the inflammatory responses induced by TLR agonists, IL-1β, and TNF-α by targeting RelA for degradation. The shRNA-mediated downregulation of COMMD1 in cancer cells enhanced inflammatory response, generating favorable conditions for macrophage recruitment. In addition, genes associated with stemness were also upregulated in these cells, which exhibited increased potential for anchorage-independent growth. Furthermore, COMMD1 downregulation promoted in vivo tumorigenesis and tumor growth, and tumors derived from COMMD1-knockdown cells displayed elevated level of NF-κB activation, increased expression of inflammatory- and stemness-associated genes, and contain expanded population of tumor-associated leukocytes and stemness-enriched cancer cells. These results suggest that COMMD1 downregulation by miR-205 promotes tumor development by modulating a positive feedback loop that amplifies inflammatory- and stemness-associated properties of cancer cells.

Indexed as

Down-RegulationAdaptor Proteins, Signal TransducingFeedback, PhysiologicalHumansInflammationMicroRNAsNeoplasmsTumor Cells, CulturedAdaptor Proteins, Signal TransducingCOMMD1 protein, humanMicroRNAsMIR205, human

Identifiers

PMID26586569
PMCPMC4832103
OpenAlexW2267613560

What OpenQuestion holds

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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.