Evidence map›Paper›PMID 34714590›Full record

ArticleCancer science2022

SNHG17, as an EMT-related lncRNA, promotes the expression of c-Myc by binding to c-Jun in esophageal squamous cell carcinoma.

Supeng Shen, Jia Liang, Xiaoliang Liang, Gaoyan Wang, Bo Feng, Wei Guo, Yanli Guo, Zhiming Dong

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.6field-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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
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  6. The essential roles of lncRNAs/PI3K/AKT axis in gastrointestinal tumors.Frontiers in cell and developmental biology · 2024
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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

8 authors at 1 institution in 1 country.

Supeng Shenthe Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Jia Liangthe Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Xiaoliang LiangLaboratory of Pathology, Hebei Cancer Institute, the Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Gaoyan Wangthe Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Bo FengLaboratory of Pathology, Hebei Cancer Institute, the Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Wei GuoLaboratory of Pathology, Hebei Cancer Institute, the Fourth Hospital of Hebei Medical University, Shijiazhuang, China.ORCID https://orcid.org/0000-0001-9690-161X
Yanli Guothe Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Zhiming Dongthe Fourth Hospital of Hebei Medical University, Shijiazhuang, China.ORCID https://orcid.org/0000-0002-7884-935X
Hebei Medical University · CN

Funding

Natural Science Foundation of Hebei Province, China H2019206664This study was supported by Grants from the National Natural Science Foundation 81472335This study was supported by Grants from the National Natural Science Foundation 81772612
6 · The paper itself

Abstract

Dysregulation of long noncoding RNA SNHG17 is associated with the occurrence of several tumors; however, its role in esophageal squamous cell carcinoma (ESCC) remains obscure. The present study demonstrated that SNHG17 was upregulated in ESCC tissues and cell lines, induced by TGF-β1, and associated with poor survival. It is also involved in the epithelial-to-mesenchymal transition (EMT) process. The mechanism underlying SNHG17-regulated c-Myc was detected by RNA immunoprecipitation, RNA pull-down, chromatin immunoprecipitation, and luciferase reporter assays. SNHG17 was found to directly regulate c-Myc transcription by binding to c-Jun protein and recruiting the complex to specific sequences of the c-Myc promoter region, thereby increasing its expression. Moreover, SNHG17 hyperactivation induced by TGF-β1 results in PI3K/AKT pathway activation, promoting cells EMT, forming a positive feedback loop. Furthermore, SNHG17 facilitated ESCC tumor growth in vivo. Overall, this study demonstrated that the SNHG17/c-Jun/c-Myc axis aggravates ESCC progression and EMT induction by TGF-β1 and may serve as a new therapeutic target for ESCC.

Indexed as

AnimalsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaFemaleGene Expression Regulation, NeoplasticHumansMaleMiceNeoplasm StagingNeoplasm TransplantationProto-Oncogene Proteins c-junProto-Oncogene Proteins c-mycJUN protein, humanMYC protein, humanProto-Oncogene Proteins c-junProto-Oncogene Proteins c-mycRNA, Long Noncodingc-MycEMTesophageal squamous cell carcinomametastasisSNHG17

Identifiers

PMID34714590
PMCPMC8748231
OpenAlexW3208818789

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.