Evidence map›Paper›PMID 30569514›Full record

ArticleJournal of cellular physiology2019

Coexpression of UCA1 and ITGA2 in pancreatic cancer cells target the expression of miR-107 through focal adhesion pathway.

Jun Gong, Xiangyu Lu, Jian Xu, Wei Xiong, Hao Zhang, Xiaojiong Yu

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

35 citing papers in PubMed, 47 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

6 authors at 1 institution in 1 country.

Jun GongDepartment of Hepatobiliary and Pancreatic Surgery, Sichuan Medical Academy & Sichuan People's Hospital, Chengdu, China.
Xiangyu LuDepartment of Hepatobiliary and Pancreatic Surgery, Sichuan Medical Academy & Sichuan People's Hospital, Chengdu, China.
Jian XuDepartment of Hepatobiliary and Pancreatic Surgery, Sichuan Medical Academy & Sichuan People's Hospital, Chengdu, China.
Wei XiongDepartment of Hepatobiliary and Pancreatic Surgery, Sichuan Medical Academy & Sichuan People's Hospital, Chengdu, China.
Hao ZhangDepartment of Hepatobiliary and Pancreatic Surgery, Sichuan Medical Academy & Sichuan People's Hospital, Chengdu, China.
Xiaojiong YuDepartment of Hepatobiliary and Pancreatic Surgery, Sichuan Medical Academy & Sichuan People's Hospital, Chengdu, China.
Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesAbnormal expressions of microRNAs (miRNAs) are demonstrated in pancreatic cancer (PaC), but a major part of the mechanism remains elusive. This study mainly aimed to structure a coexpressed network of long noncoding RNA (lncRNA) and messenger RNA (mRNA) in PaC, as well as to explore their direct targets.

methodsLncRNA and mRNA microarrays were used to determine the expression profiles in PaC cells. Analysis of Kyoto Encyclopedia of Genes and Genomes pathway was performed to identify pathways associated with differentially expressed mRNAs. Coexpression profiles were identified by constructing differentially expressed lncRNA-mRNA regulatory network and further validated by quantitative real-time polymerase chain reaction assay and western blot assay. The bioinformatics computational method was applied to predict the biological target of lncRNA and mRNA, which was identified by luciferase reporter assay. Migration/invasion ability and apoptosis rate of cells were assessed by transwell assay and flow cytometry assay.

resultsIt was identified that the level of urothelial cancer associated 1 (UCA1) was increased in PaC cells, and the inhibition of UCA1 suppressed migration and invasion ability of the cancer cells. The luciferase reporter assay recognized that miR-107 was targeted by UCA1, and integrin subunit α 2 (ITGA2) was further targeted by miR-107. This confirmed the prediction of lncRNA-miRNA-mRNA regulation mechanism. In the regulatory pathways, UCA1 and ITGA2 promoted PaC progression via focal adhesion pathway related proteins such as ITGA3, SRC protooncogene/nonreceptor tyrosine kinase, protein tyrosine kinase 2, and AKT serine/threonine kinase 1.

conclusionThe study revealed a regulatory network of UCA1-miR-107-ITGA2 and validated UCA1 and ITGA2 as potential prognostic factors for PaC.

Indexed as

ApoptosisCell Line, TumorCell MovementCell ProliferationFocal AdhesionsGene Expression Regulation, NeoplasticHumansIntegrin alpha2MicroRNAsNeoplasm InvasivenessPancreatic NeoplasmsRNA, Long NoncodingIntegrin alpha2ITGA2B protein, humanMicroRNAsMIRN107 microRNA, humanRNA, Long NoncodingUCA1 RNA, humanITGA2lncRNAsmiR-107pancreatic cancer cellsUCA1

Identifiers

PMID30569514
PMCPMC13483230
OpenAlexW2905826594

What OpenQuestion holds

Textmetadata
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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.