Evidence map›Paper›PMID 33654431›Full record

ArticleCancer management and research2021

Silencing of LncRNA SNHG16 Downregulates Cyclin D1 (CCND1) to Abrogate Malignant Phenotypes in Oral Squamous Cell Carcinoma (OSCC) Through Upregulating miR-17-5p.

Qiuling Wang, Jingxin Han, Pu Xu, Xinchun Jian, Xieshan Huang, Deyu Liu

RetractedOpen access · goldAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer management and research, 2021. 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 It has been retracted, and should not be counted.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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 19 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Qiuling Wang *Stomatology Center, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, Hainan, 570208, People's Republic of China.
Jingxin Han *Stomatology Center, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, Hainan, 570208, People's Republic of China.
Pu XuStomatology Center, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, Hainan, 570208, People's Republic of China.
Xinchun JianStomatology Center, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, Hainan, 570208, People's Republic of China.
Xieshan HuangStomatology Center, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, Hainan, 570208, People's Republic of China.
Deyu LiuStomatology Center, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, Hainan, 570208, People's Republic of China.ORCID 0000-0002-5528-3306
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTargeting the long non-coding RNAs (LncRNAs)-microRNAs (miRNAs)-mRNA competing endogenous RNA (ceRNA) networks has been proved as an effective strategy to treat multiple cancers, including oral squamous cell carcinoma (OSCC). Based on this, the present study identified a novel LncRNA SNHG16/miR-17-5p/CCND1 signaling pathway that played an important role in regulating the pathogenesis of OSCC.

methodsThe expression levels of cancer-associated genes were examined by Real-Time qPCR and Western Blot at transcriptional and translated levels, respectively. CCK-8 assay was performed to determine cell proliferation, and cell apoptosis ratio was measured by the Annexin V-FITC/PI double staining assay. Transwell assay was performed to examine cell migration, and dual-luciferase reporter gene system assay was used to validate the ceRNA networks.

resultsLncRNA SNHG16 and CCND1 were upregulated, while miR-17-5p was downregulated in OSCC tissues and cell lines, compared to their normal counterparts. Also, miR-17-5p negatively correlated with both LncRNA SNHG16 and CCND1 mRNA, but LncRNA SNHG16 was positively relevant to CCND1 mRNA in OSCC tissues. By performing the gain- and loss-of-function experiments, we noticed that LncRNA SNHG16 overexpression aggravated the malignant phenotypes, such as cell proliferation, viability, migration and epithelial-mesenchymal transition (EMT) in OSCC cells, while LncRNA SNHG16 knock-down had opposite effects. Furthermore, our dual-luciferase reporter gene system evidenced that LncRNA SNHG16 sponged miR-17-5p to upregulate CCND1 in OSCC cells, and the inhibiting effects of LncRNA SNHG16 ablation on OSCC progression were abrogated by both downregulating miR-17-5p and overexpressing CCND1. Finally, the xenograft tumor-bearing mice models were established, and our data validated that LncRNA SNHG16 served as an oncogene to promote tumorigenicity of OSCC cells in vivo.

conclusionTaken together, targeting the LncRNA SNHG16/miR-17-5p/CCND1 axis hindered the development of OSCC, and this study provided potential diagnostic and therapeutic biomarkers for OSCC in clinic.

Indexed as

competing endogenous RNAcyclin D1LncRNA SNHG16MiR-17-5poral squamous cell carcinoma

Identifiers

PMID33654431
PMCPMC7910113
OpenAlexW3130910244

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.