Evidence map›Paper›PMID 33782812›Full record

ArticleBreast cancer research and treatment2021

LncRNA SNHG6 promotes breast cancer progression and epithelial-mesenchymal transition via miR-543/LAMC1 axis.

You-Quan Wang, Guo Huang, Juan Chen, Hong Cao, Wen-Ting Xu

Open access · bronzeAbstract readEditorial
PubMed Publisher
In one paragraph

Article in Breast cancer research and treatment, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Journal of hepatocellular carcinoma · 2026
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  11. LncRNA SNHG6 role in clinicopathological parameters in cancers.European journal of medical research · 2023
    Review
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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.

You-Quan WangDepartment of Breast and Thyroid Surgery, The Second Affiliated Hospital of University of South China, No. 35 Jiefang Avenue, Fengxiang District, Hengyang, 421001, Hunan province, China. wangyquan94@163.com.ORCID http://orcid.org/0000-0001-5191-031X
Guo HuangHengyang Medical College, University of South China, Hengyang, 421001, Hunan province, China.
Juan ChenDepartment of Radiotherapy, The Second Affiliated Hospital of University of South China, Hengyang, 421001, Hunan province, China.
Hong CaoDepartment of Breast and Thyroid Surgery, The Second Affiliated Hospital of University of South China, No. 35 Jiefang Avenue, Fengxiang District, Hengyang, 421001, Hunan province, China.
Wen-Ting XuDepartment of Breast and Thyroid Surgery, The Second Affiliated Hospital of University of South China, No. 35 Jiefang Avenue, Fengxiang District, Hengyang, 421001, Hunan province, China.
University of South China · CN

Funding

Clinical Research Center for Breast & Thyroid Disease Prevention in Hunan Province 2018SK4001The Guiding Project of Clinical Medical Technology Innovation in Hunan Province 2018SK51513
6 · The paper itself

Abstract

purposeBreast cancer (BC) is the most prevalent cancer in women with an estimated incidence of 10% and the leading cause of mortality due to its heterogenous property and high metastasis rate. Development of novel therapy is very necessary and requires an understanding of molecular mechanisms. We investigated the function of SNHG6/miR-543/LAMC1 axis in BC.

methodsHuman BC tissues were obtained from diagnosed patients. BC cell lines and normal breast cells were used. QRT-PCR and Western blotting were employed to measure expression levels of SNHG6, miR-543, LAMC1, EMT-related proteins, and PI3K/AKT pathway. Dual-luciferase assay was performed to validate interactions of SNHG6/miR-543 and miR-543/LAMC1. Colony formation assay, flow cytometry, scratch wound healing assay, and transwell assay were utilized to assess the proliferation, apoptosis, migration, and invasion of BC cells. Nude mouse xenograft model was used the evaluate the function of SNHG6/miR-543 in tumor growth in vivo.

resultsSNHG6 and LAMC1 were elevated, but miR-543 was reduced in BC tissues and cells. SNHG6 interacted directly with miR-543, while miR-543 targeted LAMC1. Knockdown of SNHG6 suppressed BC cell proliferation, migration, invasion, EMT, and PI3K/AKT pathway, but promoted cell apoptosis, while miR-543 inhibitor or overexpression of LAMC1 reversed those effects. Overexpression of LAMC1 also blocked the effects of miR-543 on BC cell proliferation, migration, invasion, and EMT. Knockdown of SNHG6 restrained BC growth in vivo, while miR-543 inhibitor inhibited that suppression.

conclusionSNHG6 promoted EMT and BC cell proliferation and migration by acting as a miR-543 sponge and disinhibiting LAMC1/PI3K/AKT pathway. SNHG6/miR-543/LAMC1 axis could serve as candidates for the development of therapeutic strategies for BC.

Indexed as

Breast NeoplasmsMicroRNAsRNA, Long NoncodingCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessPhosphatidylinositol 3-KinasesMicroRNAsMIRN543 microRNA, humanPhosphatidylinositol 3-KinasesRNA, Long NoncodingBreast cancerEMTLAMC1MiR-543SNHG6

Identifiers

PMID33782812
OpenAlexW3144643921

What OpenQuestion holds

Textmetadata
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.