Evidence map›Paper›PMID 31310044›Full record

ArticleCell proliferation2019

Long non-coding RNA HCG11 modulates glioma progression through cooperating with miR-496/CPEB3 axis.

Yangzong Chen, Chunchun Bao, Xiuxing Zhang, Xinshi Lin, Hongou Huang, Zhiqiang Wang

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Cell proliferation, 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 It has been retracted, and should not be counted.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 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.2field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Long Non-Coding RNAIranian journal of public health · 2024
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. MicroRNA-3148 inhibits glioma by decreasingExperimental and therapeutic medicine · 2022
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Yangzong ChenDepartment of Radiology, Division of PET/CT, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID https://orcid.org/0000-0001-6847-4331
Chunchun BaoDepartment of Radiology, Division of PET/CT, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Xiuxing ZhangDepartment of Radiology, Division of PET/CT, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Xinshi LinDepartment of Radiology, Division of PET/CT, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Hongou HuangDepartment of Radiology, Division of PET/CT, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Zhiqiang WangDepartment of Radiology, Division of PET/CT, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesIt has been widely reported that long non-coding RNAs (lncRNAs) can participate in multiple biological processes of human cancers. lncRNA HLA complex group 11 (HCG11) has been reported in human cancers as a tumour suppressor. This study focused on investigating the function and mechanism of HCG11 in glioma. MATERIALS AND

methodsBased on The Cancer Genome Atlas (TCGA) data set and qRT-PCR analysis, the expression pattern of HCG11 was identified in glioma samples. The mechanism associated with HCG11 downregulation was determined by mechanism experiments. Gain-of-function assays were conducted for the identification of HCG11 function in glioma progression. Mechanism investigation based on the luciferase reporter assay, RIP assay and pull-down assay was used to explore the downstream molecular mechanism of HCG11. The role of molecular pathway in the progression of glioma was analysed in accordance with the rescue assays.

resultsHCG11 was expressed at low level in glioma samples compared with normal samples. FOXP1 could bind with HCG11 and transcriptionally inactivated HCG11. Overexpression of HCG11 efficiently suppressed cell proliferation, induced cell cycle arrest and promoted cell apoptosis. HCG11 was predominantly enriched in the cytoplasm of glioma cells and acted as a competing endogenous RNAs (ceRNAs) by sponging micro-496 to upregulate cytoplasmic polyadenylation element binding protein 3 (CPEB3). CEPB3 and miR-496 involved in HCG11-mediated glioma progression.

conclusionsHCG11 inhibited glioma progression by regulating miR-496/CPEB3 axis.

Indexed as

AnimalsAntagomirsApoptosisCell Cycle CheckpointsCell LineCell MovementCell ProliferationDisease ProgressionForkhead Transcription FactorsGliomaHumansMaleMiceMice, Inbred BALB CMice, NudeMicroRNAsAntagomirsCPEB3 protein, humanForkhead Transcription FactorsFOXP1 protein, humanlong noncoding RNA HCG11, humanMicroRNAsMIRN496 microRNA, humanRepressor ProteinsRNA-Binding ProteinsRNA, Long NoncodingRNA, Small InterferingCPEB3gliomaHCG11miR-496proliferation

Identifiers

PMID31310044
PMCPMC6797506
OpenAlexW2960714002

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.