Evidence map›Paper›PMID 31488171›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

Long non-coding RNA PXN-AS1 suppresses pancreatic cancer progression by acting as a competing endogenous RNA of miR-3064 to upregulate PIP4K2B expression.

Jiayan Yan, Yunxi Jia, Han Chen, Wei Chen, Xiaoying Zhou

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
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  8. Optimization of CRISPR-Cas system for clinical cancer therapy.Bioengineering & translational medicine · 2023
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  17. Identification ofGenes · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Jiayan YanDepartment of Biliary-Pancreatic Surgery, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, 200127, China.
Yunxi JiaDepartment of endoscopy of geriatric gastroenterology, First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Han ChenDepartment of gastroenterology, First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Wei ChenDepartment of Biliary-Pancreatic Surgery, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, 200127, China.
Xiaoying ZhouDepartment of gastroenterology, First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China. zhouxiaoying@yahoo.com.
Jiangsu Province Hospital · CNRenji Hospital · CNNanjing Medical University · CN

Funding

Natural Science Foundation of Jiangsu Province BK20171081
6 · The paper itself

Abstract

backgroundDysregulation of microRNAs (miRNAs) play critical roles in cancerous processes. Although miR-3064 was reported to be an important tumor suppressor in ovarian cancer, the cellular impact of miR-3064 on pancreatic cancer (PC) progression, its downstream target genes and upstream mechanisms that control the expression of miR-3064 remain to be fully clarified.

methodsWe compared miRNA expression profiles between PC tissues compared with normal tissues using a miRNA microarray analysis of clinical samples, and screened the identified miRNAs for their influence on cell proliferation. We measured the expression of miR-3064 in PC tissues and PC cell lines using quantitative real-time PCR assays. Gain- and loss-of-function experiments were conducted to explore the biologic significance of miR-3064 in PC progression both in vitro and in vivo. The interactions between miR-3064 and long noncoding RNA (lncRNA) PXN-AS1 was verified using the luciferase reporter assay and RNA immunoprecipitation assay.

resultsWe showed that miR-3064 was significantly overexpressed in PC tissues compared to normal tissues. High miR-3064 was associated with worse prognosis in patients with PC. Functionally, ectopic expression of miR-3064 promoted the proliferation, invasion, clone formation and sphere formation of PC cells in vitro and stimulated PC growth in vivo, while specific knockdown of miR-3064 or CRISPR/Cas9-mediated knockout of miR-3064 resulted in opposite phenotypes. Further investigation revealed that miR-3064 directly targeted PIP4K2B, which was reduced in PC tissues and attenuated PC cell proliferation, invasion and sphere formation induced by miR-3064. Importantly, lncRNA PXN-AS1 expression was downregulated in PC samples, and it directly interacted with miR-3064 and suppressed its levels in PC cells. Enforced expression of PXN-AS1 remarkably decreased cell proliferation, invasion and sphere formation, while re-expression of miR-3064 abrogated these effects of PXN-AS1.

conclusionsMiR-3064, a key oncogenic miRNA, could promote PC cell growth, invasion and sphere formation via downregulating the levels of tumor suppressor PIP4K2B. PXN-AS1 functioned as a sponge to suppress the expression of miR-3064. These observations offer fresh insight into the mechanisms through which miR-3064 modulates the development of PC.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedAnimalsCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalFemaleGene Expression ProfilingHumansMaleMiceMicroRNAsMiddle AgedNeoplasm MetastasisMicroRNAsMIRN-3064 microRNA, humanPhosphotransferases (Alcohol Group Acceptor)PXN-AS1 non-coding RNA, humanRNA, Long NoncodingmiR-3064Pancreatic cancerPIP4K2BPXN-AS1

Identifiers

PMID31488171
PMCPMC6727519
OpenAlexW2972254280

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.