Evidence map›Paper›PMID 27065335›Full record

ArticleOncogene2016

Downregulated miR-506 expression facilitates pancreatic cancer progression and chemoresistance via SPHK1/Akt/NF-κB signaling.

J Li, H Wu, W Li, L Yin, S Guo, X Xu, Y Ouyang, Z Zhao, S Liu, Y Tian and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 4 pooled it
12.1field-weighted citation impact, top 1% 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

101 citing papers in PubMed, 4 syntheses or guidelines pooled it, 177 citations in OpenAlex.

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41 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

J LiInstitute of Hepatopancreatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
H WuDepartment of Pancreatic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
W LiDepartment of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China.
L YinInstitute of Hepatopancreatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
S GuoInstitute of Hepatopancreatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
X XuInstitute of Hepatopancreatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
Y OuyangInstitute of Hepatopancreatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
Z ZhaoInstitute of Hepatopancreatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
S LiuInstitute of Hepatopancreatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
Y TianInstitute of Immunology PLA, Third Military Medical University, Chongqing, China.
Z TianInstitute of Immunology PLA, Third Military Medical University, Chongqing, China.
J JuTranslational Research Laboratory, Department of Pathology, Stony Brook University, Stony Brook, NY, USA.
B NiDepartment of Pathophysiology and High Altitude Pathology, Third Military Medical University, Chongqing, China.
H WangInstitute of Hepatopancreatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
Army Medical University · CNSouthwest Hospital · CNStony Brook University · US

Funding

Roles of miR-129 in colorecal cancerR01CA197098 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI JU, JINGFANG · 2016 to 2020
$1.8M
NCI NIH HHS R01 CA197098
6 · The paper itself

Abstract

The aberrant expression of microRNAs (miRNAs) has emerged as an important hallmark of cancer. However, the molecular mechanisms underlying the changes in miRNA expression remain unclear. In this study, we discovered a novel epigenetic mechanism of miR-506 regulation and investigated its functional significance in pancreatic cancer. Sequencing analysis revealed that the miR-506 promoter is highly methylated in pancreatic cancer tissues compared with non-cancerous tissues. Reduced miR-506 expression was significantly associated with clinical stage, pathologic tumor status, distant metastasis and decreased survival of pancreatic cancer patients. miR-506 inhibited cell proliferation, induced cell cycle arrest at the G1/S transition and enhanced apoptosis and chemosensitivity of pancreatic cancer cells. Furthermore, we identified sphingosine kinase 1 (SPHK1) as a novel target of miR-506, the expression of which inhibited the SPHK1/Akt/NF-κB signaling pathway, which is activated in pancreatic cancer. High SPHK1 expression was significantly associated with poor survival in a large cohort of pancreatic cancer specimens. Our data suggest that miR-506 acts as a tumor suppressor miRNA and is epigenetically silenced in pancreatic cancer. The newly identified miR-506/SPHK1 axis represents a novel therapeutic strategy for future pancreatic cancer treatment.

Indexed as

Gene Expression Regulation, Neoplastic3' Untranslated RegionsAnimalsApoptosisBinding SitesCell CycleCell Cycle CheckpointsCell Line, TumorCell ProliferationDisease Models, AnimalDisease ProgressionDrug Resistance, NeoplasmFemaleHumansMicroRNAsNF-kappa B3' Untranslated RegionsMicroRNAsMIRN506 microRNA, humanNF-kappa BPhosphotransferases (Alcohol Group Acceptor)Proto-Oncogene Proteins c-aktSphingosine Kinase

Identifiers

PMID27065335
PMCPMC5078861
OpenAlexW2339466004

What OpenQuestion holds

Textmetadata
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.