Evidence map›Paper›PMID 25010867›Full record

ArticleBritish journal of cancer2014

Downregulated miR-646 in clear cell renal carcinoma correlated with tumour metastasis by targeting the nin one binding protein (NOB1).

W Li, M Liu, Y Feng, Y-F Xu, Y-F Huang, J-P Che, G-C Wang, X-D Yao, J-H Zheng

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

47 citing papers in PubMed, 71 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

9 authors at 3 institutions in 2 countries.

W LiDepartment of Urology, Shanghai Tenth People's Hospital, Tongji University, Shanghai 200072, China.
M LiuDepartment of Urology, Shanghai Tenth People's Hospital, Tongji University, Shanghai 200072, China.
Y FengDepartment of Nephrology, Nanjing University Affiliated Drum Tower Hospital, Nanjing, Jiangsu 210093, China.
Y-F XuDepartment of Urology, Shanghai Tenth People's Hospital, Tongji University, Shanghai 200072, China.
Y-F HuangDepartment of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, FL 32603, USA.
J-P CheDepartment of Urology, Shanghai Tenth People's Hospital, Tongji University, Shanghai 200072, China.
G-C WangDepartment of Urology, Shanghai Tenth People's Hospital, Tongji University, Shanghai 200072, China.
X-D YaoDepartment of Urology, Shanghai Tenth People's Hospital, Tongji University, Shanghai 200072, China.
J-H ZhengDepartment of Urology, Shanghai Tenth People's Hospital, Tongji University, Shanghai 200072, China.
Shanghai Tenth People's Hospital · CNTongji University · CNUniversity of Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNin one binding protein (NOB1) was identified as a potential oncogene in human glioma and miR-646 plays an important role in human growth and development. However, the underlying molecular mechanisms of NOB1 in tumorigenicity and its correlation with miR-646 in renal cell carcinoma (RCC) have not been investigated.

methodsWe performed bioinformatic analysis to explore miRNA targeting NOB1. The expression of NOB1 and miR-646 from 100 cases of clear cell RCC (ccRCC) and 30 cases of adjacent non-tumour tissues were detected by quantitative real-time PCR. The expression of miR-646 was correlated with NOB1 expression, tumour features and patient metastasis-free survival. The effect of overexpression of mir-646 on renal cancer cell proliferation was detected by colony formation in soft agar. Using a xenograft tumour model, we observed the in vivo tumorigenesis effect of miR-646 and NOB1.

resultsmiR-646 negatively regulated NOB1 and inhibited the proliferation and migration of renal cancer cells. There was a significant upregulation of NOB1 in ccRCC and it was further increased in metastatic cases, while miR-646 was downregulated in tumour tissues and further decreased in metastatic ccRCC. Additionally, expression of miR-646 was inversely correlated with the expression of NOB1. The downregulation of miR-646 also indicated a higher probability of developing metastasis. Most importantly, miR-646 expression was an independent predictor of ccRCC metastasis by the univariate analysis and binary logistic regression model (both P<0.05). Colony formation in soft agar and xenograft tumour model suggested that miR-646 and NOB1 are required for tumorigenesis in vitro and in vivo. Furthermore, suppression of NOB1 increased the phosphorylation of several proteins in MAPK pathway.

conclusionsDownregulated miR-646 in ccRCC was associated with tumour metastasis through MAPK pathway by targeting NOB1. miR-646 and NOB1 may play an important role in the development of ccRCC.

Indexed as

AdultAnimalsApoptosisCarcinogenesisCarcinoma, Renal CellCell Line, TumorCell MovementCell ProliferationComputational BiologyDown-RegulationFemaleGene Expression Regulation, NeoplasticHEK293 CellsHumansKaplan-Meier EstimateKidney NeoplasmsMicroRNAsMIRN646 microRNA, humanMitogen-Activated Protein KinasesNOB1 protein, humanNuclear ProteinsRNA-Binding Proteins

Identifiers

PMID25010867
PMCPMC4453839
OpenAlexW2094428504

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.