Evidence map›Paper›PMID 28817833›Full record

ArticleBritish journal of cancer2017

FMNL2 destabilises COMMD10 to activate NF-κB pathway in invasion and metastasis of colorectal cancer.

S S Yang, X M Li, M Yang, X L Ren, J L Hu, X H Zhu, F F Wang, Z C Zeng, J Y Li, Z Q Cheng and 4 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

25 citing papers in PubMed, 44 citations in OpenAlex.

  1. METTL3-mediated mJournal of translational medicine · 2026
    Article
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  4. COMMD10 inhibited DNA damage to promote the progression of gastric cancer.Journal of cancer research and clinical oncology · 2024
    Article
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  6. Review
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  13. COMMD3 Expression Affects Angiogenesis through the HIF1Oxidative medicine and cellular longevity · 2022
    Article
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  16. Review
  17. Article
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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

14 authors at 4 institutions in 1 country.

S S YangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, Guangdong Province, People's Republic of China.
X M LiDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, Guangdong Province, People's Republic of China.
M YangDepartment of Radiotherapy, Nanfang Hospital, Southern Medical University, Guangzhou 510515, Guangdong Province, People's Republic of China.
X L RenDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, Guangdong Province, People's Republic of China.
J L HuDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, Guangdong Province, People's Republic of China.
X H ZhuDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, Guangdong Province, People's Republic of China.
F F WangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, Guangdong Province, People's Republic of China.
Z C ZengDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, Guangdong Province, People's Republic of China.
J Y LiDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, Guangdong Province, People's Republic of China.
Z Q ChengDepartment of Pathology, Shenzhen people's Hospital, Second Clinical Medical College of Jinan University, Shenzhen 518020, Guangdong Province, People's Republic of China.
W T LiaoDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, Guangdong Province, People's Republic of China.
Y Q DingDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, Guangdong Province, People's Republic of China.
J GuanDepartment of Radiotherapy, Nanfang Hospital, Southern Medical University, Guangzhou 510515, Guangdong Province, People's Republic of China.
L LiangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, Guangdong Province, People's Republic of China.
Key Laboratory of Guangdong Province · CNSouthern Medical University · CNNanfang Hospital · CNShenZhen People’s Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiaphanous-related formins (DRFs), actin necleator, have been known to participate in the progression of cancer cells. We previously reported that FMNL2 (Formin-like2), a member of DRFs, was a positive regulator in colorectal cancer (CRC) metastasis, yet proteins and pathways required for the function of this pro-invasive DRFs remain to be identified.

methodsThe relationship between FMNL2 and COMMD10 was examined using Co-IP, GST pull-down, immunofluorescence and in vitro ubiquitination assay. The in vitro and in vivo function of COMMD10 in CRC was evaluated using CCK-8 proliferation assay, plate colony formation, cell cycle, apoptosis and animal models. The inhibition of NF-κB signalling by COMMD10 was detected using dual-luciferase reporter assay and western blotting. Co-IP, GST pull-down and nuclear protein extraction assay were performed to evaluate the effect on p65 by COMMD10. Real-time PCR and western blotting were performed to detect expressions of FMNL2, COMMD10 and p65 in paired tissues.

resultsFMNL2 targets COMMD10 for ubiquitin-mediated proteasome degradation in CRC cells. COMMD10 targets p65 NF-κB (nuclear factor-κB) subunit and reduces its nuclear translocation, thereby leading to the inactivation of NF-κB pathway and suppression of CRC invasion and metastasis. Inhibition of NF-κB signalling by COMMD10 is necessary for FMNL2-mediated CRC cell behaviours. Downregulation of COMMD10 predicts poor prognosis of CRC patients. The expressions of FMNL2, COMMD10 and p65 are highly linked in CRC tissues.

conclusionsThese data demonstrate that the FMNL2/COMMD10/p65 axis acts as a critical regulator in the maintenance of metastatic phenotypes and is strongly associated with negative clinical outcomes.

Indexed as

ApoptosisBlotting, WesternCarcinomaCell MovementCell ProliferationColorectal NeoplasmsFluorescent Antibody TechniqueForminsHumansImmunoblottingImmunoprecipitationIntracellular Signaling Peptides and ProteinsIn Vitro TechniquesNeoplasm InvasivenessNeoplasm MetastasisNeoplasm TransplantationCOMMD10 protein, humanFMNL2 protein, humanForminsIntracellular Signaling Peptides and ProteinsNF-kappa BProteasome Endopeptidase ComplexProteinsRELA protein, humanTranscription Factor RelA

Identifiers

PMID28817833
PMCPMC5674093
OpenAlexW2749011160

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.