Evidence map›Paper›PMID 33298070›Full record

ArticleCancer cell international2020

ETS1-activated SNHG10 exerts oncogenic functions in glioma via targeting miR-532-3p/FBXL19 axis.

Lide Jin, Shengquan Huang, Congjin Guan, Shun Chang

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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. A functional NKILA variant (rs2273534) drives genetic susceptibility and oncogenic progression in gastric cancer via the miR-4424/OAS2 pathway.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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

4 authors at 1 institution in 1 country.

Lide JinThe First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, No.157 Jinbi Road, Kunming, 650032, Yunnan, China.
Shengquan HuangThe First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, No.157 Jinbi Road, Kunming, 650032, Yunnan, China.
Congjin GuanThe First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, No.157 Jinbi Road, Kunming, 650032, Yunnan, China. 275009026@qq.com.
Shun ChangThe First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, No.157 Jinbi Road, Kunming, 650032, Yunnan, China. stone1983712@163.com.ORCID http://orcid.org/0000-0001-7249-4108
Kunming University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn past few years, long non-coding RNAs (lncRNAs) have been reported to play regulatory roles during cancer progression. LncRNA SNHG10 has been explored in several sorts of cancers. However, its detailed role and mechanism are still not well understood in glioma.

methodsExpression levels of genes were evaluated by RT-qPCR. EdU, TUNEL, sphere formation, wound healing and transwell assays appraised the effect of SNHG10 on glioma cellular processes. The interaction between molecules was examined by ChIP, RIP, RNA pull down and luciferase reporter assays.

resultsHigh level of SNHG10 was detected in glioma cells. Functional assay confirmed that SNHG10 promoted the proliferation, migration, invasion and stemness of glioma cells. Moreover, miR-532-3p was validated to bind with SNHG10 and expressed at a low level in glioma cells. Importantly, miR-532-3p exerted inhibitory functions in glioma. Furthermore, it was found that FBXL19 targeted by miR-532-3p facilitated cell growth and stemness in glioma, and that SNHG10 worked in glioma by increasing FBXL19 expression through sequestering miR-532-3p. More importantly, ETS1 promoted the transcription of SNHG10 and it mediated contribution to the malignant behaviors of glioma cells by SNHG10/miR-532-3p/FBXL19 signaling.

conclusionSNHG10 was transcriptionally activated by ETS1 and played an oncogenic role in glioma by sponging miR-532-3p and up-regulating FBXL19.

Indexed as

ETS1FBXL19GliomamiR-532-3pSNHG10

Identifiers

PMID33298070
PMCPMC7725120
OpenAlexW3111465230

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.