Evidence map›Paper›PMID 32565736›Full record

ArticleCancer cell international2020

Long non-coding RNA SNHG22 facilitates the malignant phenotypes in triple-negative breast cancer via sponging miR-324-3p and upregulating SUDS3.

Xuan Fang, Jin Zhang, Chunyan Li, Jinjin Liu, Zhendong Shi, Peng Zhou

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

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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 1 institution in 1 country.

Xuan FangThe Third Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, West Huan-Hu Rd., Ti Yuan Bei, Hexi District, Tianjin, 300060 People's Republic of China.
Jin ZhangThe Third Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, West Huan-Hu Rd., Ti Yuan Bei, Hexi District, Tianjin, 300060 People's Republic of China.ORCID 0000-0001-8938-1062
Chunyan LiThe Third Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, West Huan-Hu Rd., Ti Yuan Bei, Hexi District, Tianjin, 300060 People's Republic of China.
Jinjin LiuThe Third Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, West Huan-Hu Rd., Ti Yuan Bei, Hexi District, Tianjin, 300060 People's Republic of China.
Zhendong ShiThe Third Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, West Huan-Hu Rd., Ti Yuan Bei, Hexi District, Tianjin, 300060 People's Republic of China.
Peng ZhouThe Third Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, West Huan-Hu Rd., Ti Yuan Bei, Hexi District, Tianjin, 300060 People's Republic of China.
Tianjin Medical University Cancer Institute and Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreasing evidence has indicated the important role of long non-coding RNAs (lncRNAs) in regulating the development and progression of cancers, including triple-negative breast cancer (TNBC). Small nucleolar RNA host gene 22 (SNHG22) is a novel lncRNA that has been identified as tumor-contributor in ovarian carcinoma. However, its function has not been explored in TNBC.

methodsqRT-PCR was used to identify gene expression at mRNA level while western blot was utilized to analyze the protein level. Functional assays were implemented to identify changes on the proliferation, apoptosis and motility of TNBC cells under different conditions. Additionally, mechanistic assays, such as RIP assay, RNA pull down assay and luciferase reporter assay, were applied to assess relationships between molecules.

resultsSNHG22 represented a high expression level in TNBC tissues and cells. Besides, SNHG22 silencing restrained the proliferation, migration and invasion of TNBC cells. Furthermore, miR-324-3p that was lowly expressed in TNBC cells was conformed to be sponged by SNHG22. Moreover, upregulated miR-324-3p inhibited cell proliferation and motility in TNBC. Subsequently, we identified that SUDS3, a tumor-facilitator with elevated expression in TNBC, was the downstream target of SNHG22/miR-324-3p axis. Of note, miR-324-3p repression or SUDS3 overexpression could rescue the anti-tumor effect of SNHG22 silencing on the malignant phenotypes of TNBC cells.

conclusionLncRNA SNHG22 facilitated cell growth and motility in TNBC via sponging miR-324-3p and upregulating SUDS3, highlighting a new promising road for TNBC treatment development.

Indexed as

miR-324-3pSNHG22SUDS3Triple-negative breast cancer

Identifiers

PMID32565736
PMCPMC7302359
OpenAlexW3036380512

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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.