Evidence map›Paper›PMID 32301277›Full record

ArticleJournal of cellular and molecular medicine2020

Down-regulated lncRNA SBF2-AS1 in M2 macrophage-derived exosomes elevates miR-122-5p to restrict XIAP, thereby limiting pancreatic cancer development.

Zi Yin, Yu Zhou, Tingting Ma, Sheng Chen, Ning Shi, Yiping Zou, Baohua Hou, Chuanzhao Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 2 pooled it
6.8field-weighted citation impact, top 2% 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

86 citing papers in PubMed, 2 syntheses or guidelines pooled it, 116 citations in OpenAlex.

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  20. Progress of Exosomal LncRNAs in Pancreatic Cancer.International journal of molecular sciences · 2024
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26 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

8 authors at 2 institutions in 1 country.

Zi YinGeneral Surgery Department, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Yu ZhouGeneral Surgery Department, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Tingting MaObstetrics and Gynecology Department, Sun Yat-Sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China.
Sheng ChenGeneral Surgery Department, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Ning ShiGeneral Surgery Department, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Yiping ZouGeneral Surgery Department, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Baohua HouGeneral Surgery Department, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Chuanzhao ZhangGeneral Surgery Department, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.ORCID 0000-0002-9782-6970
Guangdong General Hospital · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Evidence has indicated that M2 macrophages promote the progression of cancers, but few focus on the ability of M2 macrophage-derived exosomes in pancreatic cancer (PC). This study aims to explore how M2 macrophages affect malignant phenotypes of PC through regulating long non-coding RNA SET-binding factor 2 antisense RNA 1 (lncRNA SBF2-AS1)/microRNA-122-5p (miR-122-5p)/X-linked inhibitor of apoptosis protein (XIAP) axis. THP-1 cells were transformed into M1 macrophages by lipopolysaccharide and interferon-γ treatment, and into M2 macrophages after interleukin-4 treatment. The PANC-1 PC cell line with the largest lncRNA SBF2-AS1 expression was selected, and M2 macrophage-derived exosomes were isolated and identified. A number of assays were applied for the examination of lncRNA SBF2-AS1 expression, PC cell biological functions and subcellular localization of lncRNA SBF2-AS1. XIAP expression was detected, along with the interaction among lncRNA SBF2-AS1, miR-122-5p and XIAP. M2 macrophage exosomal lncRNA SBF2-AS1 expression's effects on the tumorigenic ability of PANC-1 cells in nude mice were also investigated. M2 macrophage-derived exosomes promoted progression of PC cells. Overexpressed lncRNA SBF2-AS1 promoted progression of PC cells. LncRNA SBF2-AS1 was found to act as a competing endogenous RNA to repress miR-122-5p and up-regulate XIAP. Constrained lncRNA SBF2-AS1 in M2 macrophage-derived exosomes contributed to restraining tumorigenic ability of PC cells. Collectively, our study reveals that constrained lncRNA SBF2-AS1 in M2 macrophage-derived exosomes increases miR-122-5p expression to restrain XIAP expression, which further inhibits PC progression.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCarcinogenesisCell Line, TumorDisease ProgressionExosomesFemaleHumansInhibitor of Apoptosis ProteinsIn Situ Hybridization, FluorescenceLipopolysaccharidesMacrophagesMiceMice, Inbred BALB CMice, NudeMicroRNAsBirc4 protein, mouseInhibitor of Apoptosis ProteinsLipopolysaccharidesMicroRNAsMIRN122 microRNA, humanMirn122 microRNA, mouseOligonucleotides, AntisenseProtein Tyrosine Phosphatases, Non-ReceptorRNA, Long NoncodingSBF2 protein, humanSbf2 protein, mouseXIAP protein, humanX-Linked Inhibitor of Apoptosis ProteinexosomesLncRNA SBF2-AS1macrophagesMicroRNA-122-5ppancreatic cancerX-linked inhibitor of apoptosis protein

Identifiers

PMID32301277
PMCPMC7205800
OpenAlexW3016798942

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.