Evidence map›Paper›PMID 33811437›Full record

ArticleJournal of cellular and molecular medicine2021

miR-365 secreted from M2 Macrophage-derived extracellular vesicles promotes pancreatic ductal adenocarcinoma progression through the BTG2/FAK/AKT axis.

Xin Li, Hao Xu, Jianfeng Yi, Chunlu Dong, Hui Zhang, Zhengfeng Wang, Long Miao, Wence Zhou

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
7.1field-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

23 citing papers in PubMed, 54 citations in OpenAlex.

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  17. International journal of general medicine · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Xin LiThe First Clinical Medical College, Lanzhou University, Lanzhou, China.ORCID 0000-0002-8898-9938
Hao XuThe First Clinical Medical College, Lanzhou University, Lanzhou, China.
Jianfeng YiThe First Clinical Medical College, Lanzhou University, Lanzhou, China.
Chunlu DongThe First Clinical Medical College, Lanzhou University, Lanzhou, China.
Hui ZhangDepartment of General Surgery, the First Hospital of Lanzhou University, Lanzhou, China.
Zhengfeng WangDepartment of General Surgery, the First Hospital of Lanzhou University, Lanzhou, China.
Long MiaoDepartment of General Surgery, the First Hospital of Lanzhou University, Lanzhou, China.
Wence ZhouThe First Clinical Medical College, Lanzhou University, Lanzhou, China.ORCID 0000-0003-2573-9170
First Hospital of Lanzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clinical and experimental evidence indicates that tumour-associated macrophages support cancer progression. Moreover, macrophage-derived extracellular vesicles (EVs) are involved in pathogenesis of multiple cancers, yet the functions of molecular determinants in which have not been fully understood. Herein, we aim to understand whether macrophage modulates pancreatic ductal adenocarcinoma (PDAC) progression in an EV-dependent manner and the underlying mechanisms. microRNA (miR)-365 was experimentally determined to be enriched in the EVs from M2 macrophages (M2-EVs), which could be transferred into PDAC cells. Using a co-culture system, M2-EVs could enhance the proliferating, migrating and invading potentials of PDAC cells, while inhibition of miR-365 in M2-EVs could repress these malignant functions. B-cell translocation gene 2 (BTG2) was identified to be a direct target of miR-365, while the focal adhesion kinase (F/ATP)-dependent tyrosine kinase (AKT) pathway was activated by miR-365. We further demonstrated that overexpression of BTG2 could delay the progression of PDAC in vitro, whereas by impairing BTG2-mediated anti-tumour effect, M2-EV-miR-365 promoted PDAC progression. For validation, a nude mouse model of tumorigenesis was established, in which we found that targeting M2-EV-miR-365 contributed to suppression of tumour growth. Collectively, M2-EVs carry miR-365 to suppress BTG2 expression, which activated FAK/AKT pathway, thus promoting PDAC development.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBiomarkers, TumorCarcinoma, Pancreatic DuctalCell ProliferationExtracellular VesiclesFocal Adhesion Kinase 1HumansImmediate-Early ProteinsMacrophagesMaleMiceMice, Inbred BALB CMice, NudeMicroRNAsBiomarkers, TumorBTG2 protein, humanFocal Adhesion Kinase 1Immediate-Early ProteinsMicroRNAsMIRN365 microRNA, humanProto-Oncogene Proteins c-aktPTK2 protein, humanTumor Suppressor ProteinsBTG2cell invasionextracellular vesiclesFAK/AKT pathwaymacrophagesmicroRNA-365pancreatic ductal adenocarcinoma

Identifiers

PMID33811437
PMCPMC8107105
OpenAlexW3147869548

What OpenQuestion holds

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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.