Evidence map›Paper›PMID 33187481›Full record

ArticleMolecular medicine (Cambridge, Mass.)2020

ZLM-7 inhibits the occurrence and angiogenesis of breast cancer through miR-212-3p/Sp1/VEGFA signal axis.

Xuan Li, Zi-Zheng Zou, Min Wen, Yuan-Zhu Xie, Kun-Jian Peng, Tiao Luo, Su-You Liu, Qin Gu, Ji-Jia Li, Zhi-Yong Luo

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

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  17. Multi-Omics Analysis of the Effects of Smoking on Human Tumors.Frontiers in molecular biosciences · 2021
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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

10 authors at 1 institution in 1 country.

Xuan LiMolecular Biology Research Centre, Hunan Province Key Laboratory of Basic and Applied Hematology, Hunan Key Laboratory of Animal Models for Human Diseases, School of Life Sciences, Central South University, Changsha, 410008, Hunan, China.
Zi-Zheng ZouMolecular Biology Research Centre, Hunan Province Key Laboratory of Basic and Applied Hematology, Hunan Key Laboratory of Animal Models for Human Diseases, School of Life Sciences, Central South University, Changsha, 410008, Hunan, China.
Min WenMolecular Biology Research Centre, Hunan Province Key Laboratory of Basic and Applied Hematology, Hunan Key Laboratory of Animal Models for Human Diseases, School of Life Sciences, Central South University, Changsha, 410008, Hunan, China.
Yuan-Zhu XieMolecular Biology Research Centre, Hunan Province Key Laboratory of Basic and Applied Hematology, Hunan Key Laboratory of Animal Models for Human Diseases, School of Life Sciences, Central South University, Changsha, 410008, Hunan, China.
Kun-Jian PengMolecular Biology Research Centre, Hunan Province Key Laboratory of Basic and Applied Hematology, Hunan Key Laboratory of Animal Models for Human Diseases, School of Life Sciences, Central South University, Changsha, 410008, Hunan, China.
Tiao LuoHunan Key Laboratory of Oral Health Research, Xiangya Stomatological Hospital, Xiangya School of Stomatology, Central South University, Changsha, 410008, Hunan, China.
Su-You LiuSchool of Pharmaceutical Sciences, Central South University, Changsha, 410013, China.
Qin GuMolecular Biology Research Centre, Hunan Province Key Laboratory of Basic and Applied Hematology, Hunan Key Laboratory of Animal Models for Human Diseases, School of Life Sciences, Central South University, Changsha, 410008, Hunan, China.
Ji-Jia LiXiangya Hospital, Central South University, Changsha, 410008, Hunan, China. lijijia1986@126.com.
Zhi-Yong LuoMolecular Biology Research Centre, Hunan Province Key Laboratory of Basic and Applied Hematology, Hunan Key Laboratory of Animal Models for Human Diseases, School of Life Sciences, Central South University, Changsha, 410008, Hunan, China. luozhiyong@csu.edu.cn.ORCID 0000-0002-4369-0780
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBreast cancer (BC) is a common malignant tumor with poor prognosis. Angiogenesis is related to the growth and progression of solid tumors and associated with prognosis. ZLM-7, SP1, VEGFA and miR-212-3p were associated with BC angiogenesis and proliferation, however the detailed mechanism was not clear. This study aimed to reveal the regulatory mechanism of angiogenesis of BC.

methodsBC cell lines were treated with 10 nM ZLM-7 for 8 h. We detected protein expression level by western blot and RNA expression level by qRT-PCR. Overexpression or inhibition of miR-212-3p is performed using miR-212-3p mimics or miR-212-3p inhibitor, Sp1 overexpression using pcDNA3.1 vector. Angiogenesis was analyzed by co-culturing BC cell lines and HUVEC cells. To evaluate regulatory relationship between miR-212-3p and Sp1, dual luciferase assay was performed. Besides, the direct interaction between Sp1 and VEGFA was analyzed by ChIP. Migration and invasion were analyzed by transwell assay and proliferation was detected by clone formation assay. In mice xenograft model developed using BC cells, we also detected angiogenesis marker CD31 through immunohistochemistry.

resultsZLM-7 up-regulated miR-212-3p and inhibited invasion, migration, proliferation and angiogenesis of BC, while miR-212-3p inhibitor antagonized such effects. Binding sequence was revealed between miR-212-3p and Sp1, and expression of Sp1 was inhibited by miR-212-3p on both protein and mRNA level. Sp1 could interact with VEGFA and promoted its expression. Overexpression of miR-212-3p inhibited migration, invasion, proliferation and angiogenesis of BC cell lines, while Sp1 overexpression showed the opposite effect and could antagonize these effects of miR-212-3p overexpression. ZLM-7 decreased VEGFA expression, which was rescued by co-transfection with miR-212-3p inhibitor. Similar, ZLM-7 could inhibit tumor growth and angiogenesis through the miR-212-3p/Sp1/VEGFA axis in vivo.

conclusionsZLM-7 could directly up-regulate miR-212-3p in BC. MiR-212-3p could inhibit VEGFA expression through Sp1, thereby inhibiting angiogenesis and progression of BC.

Indexed as

3' Untranslated RegionsAniline CompoundsBreast NeoplasmsCell Line, TumorCell MovementFemaleGene Expression Regulation, NeoplasticHumansMicroRNAsNeovascularization, PathologicSignal TransductionSp1 Transcription FactorSulfidesVascular Endothelial Growth Factor A3' Untranslated RegionsAniline CompoundsMicroRNAsMIRN212 microRNA, humanSp1 Transcription FactorSulfidesVascular Endothelial Growth Factor AZLM-7 compoundBreast cancermiR-212-3pSp1VEGFAZLM-7

Identifiers

PMID33187481
PMCPMC7666510
OpenAlexW3099107510

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.