Evidence map›Paper›PMID 30705598›Full record

ArticleOncoTargets and therapy2019

LncRNA SNHG16 drives proliferation and invasion of papillary thyroid cancer through modulation of miR-497.

Qiang Wen, Lina Zhao, Tongtong Wang, Ningning Lv, Xuejiao Cheng, Guang Zhang, Lin Bai

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

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  8. Tamoxifen resistance-related ceRNA network for breast cancer.Frontiers in cell and developmental biology · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Qiang WenDepartment of Nuclear Medicine, China-Japan Union Hospital of Jilin University, ErDao District, Changchun 13033, China, linbai830@tom.com.
Lina ZhaoDepartment of Thyroid Surgery, China-Japan Union Hospital of Jilin University, ErDao District, Changchun 13033, China, zhangguang_74@163.com.
Tongtong WangDepartment of Nuclear Medicine, China-Japan Union Hospital of Jilin University, ErDao District, Changchun 13033, China, linbai830@tom.com.
Ningning LvDepartment of Nuclear Medicine, China-Japan Union Hospital of Jilin University, ErDao District, Changchun 13033, China, linbai830@tom.com.
Xuejiao ChengDepartment of Nuclear Medicine, China-Japan Union Hospital of Jilin University, ErDao District, Changchun 13033, China, linbai830@tom.com.
Guang ZhangDepartment of Thyroid Surgery, China-Japan Union Hospital of Jilin University, ErDao District, Changchun 13033, China, zhangguang_74@163.com.
Lin BaiDepartment of Nuclear Medicine, China-Japan Union Hospital of Jilin University, ErDao District, Changchun 13033, China, linbai830@tom.com.
Union Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong noncoding small nucleolar RNA host gene 16 (SNHG16) has been shown to play an oncogenic role in multiple cancers. However, the biological roles and mechanism of SNHG16 action in the regulation of papillary thyroid cancer (PTC) remains unknown. The aims of this study were to investigate the roles and the possible mechanism of SNHG16 in PTC progression. MATERIALS AND

methodsThe expression of SNHG16 PTC tissues and cell lines was detected by reverse-transcription quantitative PCR (qRT-PCR). The effect of SNHG16 on cell proliferation, apoptosis, migration, and invasion was detected by Cell Counting Kit-8, flow cytometry, wound-healing assay, and Matrigel invasion assay, respectively. In addition, the regulatory relationships between SNHG16 and miR-497 were explored by luciferase reporter assay and qRT-PCR.

resultsThe SNHG16 expression was upregulated in PTC tissues and cell lines, whose expression was positively associated with advanced TNM stage and lymph node metastasis. Function analysis demonstrated that depletion of SNHG16 in PTC cells significantly inhibited cell proliferation, induced cell apoptosis, and suppressed cell migration and invasion abilities. Mechanistic studies indicated that SNHG16 functioned as an endogenous sponge for miR-497 to regulate its target genes brain-derived neurotrophic factor and yes-associated protein 1 expression. Furthermore, the inhibition of miR-497 antagonized the suppressive effect of SNHG16-depleted cells on cell proliferation, migration, and invasion.

conclusionThese findings revealed that SNHG16 drived the PTC progression possibly via regulating miR-497, suggesting that SNHG16 might be a novel therapeutic agent for PTC.

Indexed as

long noncoding RNAsmiR-497papillary thyroid cancerSNHG16

Identifiers

PMID30705598
PMCPMC6343509
OpenAlexW2911104932

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.