Evidence map›Paper›PMID 29328486›Full record

ArticleOncology reports2018

miR‑873 inhibits colorectal cancer cell proliferation by targeting TRAF5 and TAB1.

Hui Gong, Lishan Fang, Yifan Li, Jihui Du, Bei Zhou, Xiu Wang, Hekai Zhou, Lingli Gao, Kaixin Wang, Juan Zhang

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 33 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

10 authors at 3 institutions in 1 country.

Hui GongCentral Laboratory, Shenzhen Nanshan People's Hospital/Affiliated Shenzhen Sixth Hospital of Guangdong Medical University, Shenzhen, Guangdong 518033, P.R. China.
Lishan FangCentral Laboratory, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong 518033, P.R. China.
Yifan LiCentral Laboratory, Shenzhen Nanshan People's Hospital/Affiliated Shenzhen Sixth Hospital of Guangdong Medical University, Shenzhen, Guangdong 518033, P.R. China.
Jihui DuCentral Laboratory, Shenzhen Nanshan People's Hospital/Affiliated Shenzhen Sixth Hospital of Guangdong Medical University, Shenzhen, Guangdong 518033, P.R. China.
Bei ZhouCentral Laboratory, Shenzhen Nanshan People's Hospital/Affiliated Shenzhen Sixth Hospital of Guangdong Medical University, Shenzhen, Guangdong 518033, P.R. China.
Xiu WangClinical Laboratory, Shenzhen Nanshan People's Hospital/Affiliated Shenzhen Sixth Hospital of Guangdong Medical University, Shenzhen, Guangdong 518033, P.R. China.
Hekai ZhouCentral Laboratory, Shenzhen Nanshan People's Hospital/Affiliated Shenzhen Sixth Hospital of Guangdong Medical University, Shenzhen, Guangdong 518033, P.R. China.
Lingli GaoCentral Laboratory, Shenzhen Nanshan People's Hospital/Affiliated Shenzhen Sixth Hospital of Guangdong Medical University, Shenzhen, Guangdong 518033, P.R. China.
Kaixin WangDepartment of Pathology, Shenzhen Nanshan People's Hospital/Affiliated Shenzhen Sixth Hospital of Guangdong Medical University, Shenzhen, Guangdong 518033, P.R. China.
Juan ZhangDepartment of Pathology, Shenzhen Nanshan People's Hospital/Affiliated Shenzhen Sixth Hospital of Guangdong Medical University, Shenzhen, Guangdong 518033, P.R. China.
Shenzhen Sixth People's Hospital · CNGuangdong Medical College · CNEighth Affiliated Hospital of Sun Yat-sen University

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA-873 (miR‑873) has been reported to be dysregulated in a variety of malignancies, however, the biological function and underlying molecular mechanism of miR‑873 in colorectal cancer (CRC) remain unclear. In the present study we found that the expression levels of miR‑873 were markedly decreased in CRC cell lines and tissues from patients. Statistical analysis revealed that miR‑873 expression was inversely correlated with the disease stage of CRC. Kaplan‑Meier survival analysis revealed that patients with CRC with lower miR‑873 expression had shorter overall survival rates. Additionally, downregulation of miR‑873 enhanced the proliferation of CRC cells, while upregulation of miR‑873 reduced this proliferation. Furthermore, we found that tumor necrosis factor (TNF) receptor-associated factor 5 (TRAF5) and TGF‑β activated kinase 1 (MAP3K7) binding protein 1 (TAB1) were direct targets of miR‑873 in CRC cells. A luciferase assay revealed that ectopic expression of miR‑873 significantly reduced nuclear factor κB (NF‑κB) luciferase activity, while ectopic expression of miR‑873 inhibitor enhanced luciferase activity, suggesting that downregulation of miR‑873 can activate NF‑κB signaling. Therefore, our findings established a tumor-suppressive role for miR‑873 in the inhibition of CRC progression, which may be employed as a novel prognostic marker and as an effective therapeutic target for CRC.

Indexed as

Cell ProliferationGene Expression Regulation, NeoplasticAdaptor Proteins, Signal TransducingApoptosisBiomarkers, TumorColorectal NeoplasmsDisease ProgressionFemaleFollow-Up StudiesHumansMaleMicroRNAsMiddle AgedPrognosisSignal TransductionSurvival RateAdaptor Proteins, Signal TransducingBiomarkers, TumorMicroRNAsMIRN873 microRNA, humanTAB1 protein, humanTNF Receptor-Associated Factor 5TRAF5 protein, human

Identifiers

PMID29328486
PMCPMC5802030
OpenAlexW2783795123

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.