Evidence map›Paper›PMID 32705220›Full record

ArticleMolecular medicine reports2020

Long non‑coding RNA growth arrest‑specific 5 (GAS5) acts as a tumor suppressor by promoting autophagy in breast cancer.

Guangping Li, Lin Qian, Xiaoqin Tang, Yuan Chen, Ziyi Zhao, Cuiwei Zhang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2020. 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
1.5field-weighted citation impact, top 18% 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, 30 citations in OpenAlex.

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  17. Crucial Roles of LncRNAs-Mediated Autophagy in Breast Cancer.International journal of medical sciences · 2022
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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

6 authors at 2 institutions in 1 country.

Guangping Li *Integration of Traditional and Western Medicine and Oncology, Chengdu, Sichuan 610072, P.R. China.
Lin Qian *The Teaching Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 610072, P.R. China.
Xiaoqin TangDepartment of Pathology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Yuan ChenDepartment of Pathology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Ziyi ZhaoThe Teaching Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 610072, P.R. China.
Cuiwei ZhangDepartment of Pathology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Affiliated Hospital of Southwest Medical University · CNChengdu University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growth arrest‑specific 5 (GAS5) is a known tumor suppressor which negatively regulates cell survival and malignancy in several cancer cell types. The present study aimed to establish the correlation between GAS5 and unc‑51 like autophagy activating kinase (ULK)1/2, two key regulators of autophagy initiation in breast cancer (BC). To address this, expression levels of these genes were quantitively analyzed in BC clinical samples by performing reverse transcription‑quantitative PCR. GAS5 was downregulated in BC clinical samples compared with adjacent samples and was positively correlated with ULK1/2. Detection methods including cell cycle analysis, annexin V‑FITC/PI double staining and flow cytometry analysis, Transwell cell invasion assay, transfection and western blotting were used for BC cells. In MCF‑7 cells, it was also observed that overexpression of GAS5 upregulated ULK1/2 protein levels without disturbing other autophagy initiation‑associated proteins and inhibited cell proliferation, invasion and tumor formation. These effects were reversed by blocking autophagy with 3‑methyladenine (3‑MA). These results demonstrated that the suppressive effects of overexpressed GAS5 were mediated via autophagy induction, at least in part. Overexpression of GAS5 induced chemoresistance to cisplatin, which was not reversed by 3‑MA‑mediated inhibition of autophagy, indicating that GAS5 promotes chemosensitivity in an autophagy‑independent manner. Collectively, these results indicated that GAS5 contributes to the pathogenesis of BC potentially by promoting autophagy. However, the mechanism by which GAS5 functions as a tumor suppressor in an autophagy‑independent manner remains unknown.

Indexed as

AdultAgedAged, 80 and overAutophagyAutophagy-Related Protein-1 HomologBreast NeoplasmsCell Line, TumorDown-RegulationFemaleHumansIntracellular Signaling Peptides and ProteinsMCF-7 CellsMiddle AgedProtein Serine-Threonine KinasesRNA, Long NoncodingAutophagy-Related Protein-1 HomologGAS5 long non-coding RNA, humanIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesRNA, Long NoncodingULK1 protein, humanUlk2 protein, humanautophagybreast cancerchemosensitivitygrowth arrest‑specific 5unc‑51‑like autophagy activating kinase 1/2

Identifiers

PMID32705220
PMCPMC7411390
OpenAlexW3041419294

What OpenQuestion holds

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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.