Evidence map›Paper›PMID 32538432›Full record

Observational studyBioscience reports2020

LncRNA GNAS-AS1 facilitates ER+ breast cancer cells progression by promoting M2 macrophage polarization via regulating miR-433-3p/GATA3 axis.

Shi-Qin Liu, Zhi-Yang Zhou, Xue Dong, Lei Guo, Ke-Jing Zhang

Open access · goldAbstract readObservational Study
In one paragraph

Observational study in Bioscience reports, 2020. 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
3.2field-weighted citation impact, top 6% 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, 59 citations in OpenAlex.

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  11. Macrophage subtypes inhibit breast cancer proliferation in culture.bioRxiv : the preprint server for biology · 2024
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  15. LncRNA IGFL2-AS1 as a ceRNA Promotes HCT116 Cell Malignant Proliferation via the miR-433-3p/PAK4 Axis.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023
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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

5 authors at 1 institution in 1 country.

Shi-Qin LiuDepartment of General Surgery, Xiangya Hospital, Central South University, Changsha 410008, Hunan Province, P.R. China.
Zhi-Yang ZhouDepartment of General Surgery, Xiangya Hospital, Central South University, Changsha 410008, Hunan Province, P.R. China.
Xue DongDepartment of General Surgery, Xiangya Hospital, Central South University, Changsha 410008, Hunan Province, P.R. China.
Lei GuoDepartment of General Surgery, Xiangya Hospital, Central South University, Changsha 410008, Hunan Province, P.R. China.
Ke-Jing ZhangDepartment of General Surgery, Xiangya Hospital, Central South University, Changsha 410008, Hunan Province, P.R. China.
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveER+ breast cancer is the most common type of breast cancer, which seriously affects the physical and mental health of women. Recently, lncRNAs mediated tumor-associated macrophages (TAM) were identified to involve in tumorigenesis. Therefore, the present study aimed at demonstrating the regulatory network of GNAS-AS1 in TAM-mediated ER+ breast cancer progress.

methodsThe expression levels of genes were evaluated using qRT-PCR. The proportions of polarized macrophages (M1, M2) were assessed by flow cytometry. Cell proliferation, migration and invasion were evaluated by CCK-8, wound healing and transwell assay, respectively. Double-luciferase reporter system was used to detect the interaction between molecules. Western blot was applied to test protein levels.

resultsThe expression of GNAS-AS1 was obviously increased in ER+ breast cancer tissues and cell lines, as well as M2 macrophages. GNAS-AS1 facilitated the capabilities of proliferation, migration and invasion of ER+ breast cancer cells by accelerating M2 macrophage polarization via directly sponging miR-433-3p. GATA3, as a target of miR-433-3p, could positively regulate by GNAS-AS1. Furthermore, either miR-433-3p overexpression or GATA3 knockdown impaired the effects of GNAS-AS1 on M2 macrophage polarization and ER+ breast cancer cells progression.

conclusionGNAS-AS1/miR-433-3p/GATA3 axis promoted proliferation, metastasis of ER+ breast cancer cells by accelerating M2 macrophage polarization. The mechanism may provide a new strategy and target for ER+ breast cancer treatment.

Indexed as

BreastBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGATA3 Transcription FactorGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMacrophage ActivationMacrophagesMastectomyMicroRNAsNeoplasm InvasivenessGATA3 protein, humanGATA3 Transcription FactorMicroRNAsMIRN433 microRNA, humanReceptors, EstrogenRNA, Long NoncodingER+ Breast cancerGATA3GNAS-AS1Macrophage polarizationmiR-433-3p

Identifiers

PMID32538432
PMCPMC7327181
OpenAlexW3035501932

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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.