Evidence map›Paper›PMID 26019136›Full record

ArticleOncotarget2015

MicroRNA-301a-3p promotes pancreatic cancer progression via negative regulation of SMAD4.

Xiang Xia, Kundong Zhang, Gang Cen, Tao Jiang, Jun Cao, Kejian Huang, Chen Huang, Qian Zhao, Zhengjun Qiu

Abstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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, 1 synthesis or guideline pooled it.

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  15. MicroRNA-301a-3p promotes diabetic retinopathy via regulation of six-transmembrane epithelial antigen of prostate 4.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
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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.

Xiang XiaDepartment of General Surgery, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai, China.
Kundong ZhangDepartment of General Surgery, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai, China.
Gang CenDepartment of General Surgery, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai, China.
Tao JiangDepartment of General Surgery, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai, China.
Jun CaoDepartment of General Surgery, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai, China.
Kejian HuangDepartment of General Surgery, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai, China.
Chen HuangDepartment of General Surgery, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai, China.
Qian ZhaoDepartment of Pathophysiology, Key Laboratory of Cell Differentiation and Apoptosis and National Ministry of Education, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Zhengjun QiuDepartment of General Surgery, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAim to determine the clinicopathological and prognostic role of miR-301a-3p in pancreatic ductal adenocarcinoma(PDAC), to investigate the biological mechanism of miR-301a-3p in vitro and in vivo.

methodsBy tissue microarray analysis, we studied miR-301a-3p expression in PDAC patients and its clinicopathological correlations as well as prognostic significance. qRT-PCR was used to test miR-301a-3p expression in PDAC tissues and cell lines. Functional experiments including in vitro and in vivo were performed.

resultsSignificantly higher expression of miR-301a-3p were found in PDAC patients with lymph node metastasis and advanced pathological stages and identified as an independent prognostic factor for worse survival. In PDAC samples and cell lines, miR-301a-3p was significantly up-regulated compared with matched non-tumor tissues and normal pancreatic ductal cells, respectively. Overexpression of miR-301a-3p enhanced PDAC cells colony, invasion and migration abilities in vitro as well as tumorigenicity in vivo. Furthermore, SMAD4 was identified as a target gene of miR-301a-3p by cell as well as mice xenograft experiments. In PDAC tissue microarray, a significantly inverse correlation between miR-301a-3p ISH scores and SMAD4 IHC scores were observed in both tumor and corresponding non-tumor tissues.

conclusionsMiR-301a-3p functions as a novel oncogene in PDAC and the oncogenic activity may involve its inhibition of the target gene SMAD4.

Indexed as

AgedAnimalsCarcinoma, Pancreatic DuctalCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHEK293 CellsHumansImmunohistochemistryIn Situ HybridizationLymphatic MetastasisMaleMiceMice, NudeMicroRNAsMIRN301A microRNA, humanSmad4 ProteinSMAD4 protein, humanmiR-301a-3ppancreatic ductal adenocarcinomaprognosisSMAD4xenograft tumor

Identifiers

PMID26019136
PMCPMC4673249

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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.