Evidence map›Paper›PMID 34694569›Full record

ArticleHuman cell2022

LncRNA USP30-AS1 promotes the survival of acute myeloid leukemia cells by cis-regulating USP30 and ANKRD13A.

Wei Zhou, Shilin Xu, Tingfen Deng, Ruiqing Zhou, Caixia Wang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Human cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Wei ZhouDepartment of Hematology, School of Medicine, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, Guangdong, China. eyweizhou@scut.edu.cn.
Shilin XuDepartment of Hematology, School of Medicine, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, Guangdong, China.
Tingfen DengDepartment of Hematology, School of Medicine, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, Guangdong, China.
Ruiqing ZhouDepartment of Hematology, School of Medicine, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, Guangdong, China. eyzhourq@scut.edu.cn.
Caixia WangDepartment of Hematology, School of Medicine, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, Guangdong, China.
South China University of Technology · CNGuangzhou Medical University · CN

Funding

Fundamental Research Funds for the Central Universities No.2175060Natural Science Foundation of China No.81600147
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a malignant tumor derived from leukemia stem cells, with complicated pathogenesis. LncRNAs play an important role in tumors genesis and progression. According to results from bioinformatics analysis, lncRNA USP30-AS1 is highly expressed in AML and both the high expression of USP30-AS1 and low methylation level at Cg03124318 locus of USP30-AS1 gene promoter are associated with poor prognosis of AML. This study knocked down and overexpressed USP30-AS1 to determine the roles in AML cell lines. High-throughput sequencing was performed to explore the genes regulated by USP30-AS1. Results showed that USP30-AS1 promoted AML cell viability and inhibited apoptosis. Genes regulated by USP30-AS1 are mainly related to genetic regulation and immune system. Among them, USP30 and ANKRD13A genes are close to USP30-AS1 gene in chromosome. Knockdown of USP30, but not ANKRD13A, abolished the cancer-promoting effects of USP30-AS1. ANKRD13A recognizes Lys-63-linked polyubiquitin chain in HLA-I. USP30-AS1 induced HLA-I internalization from the cell membrane by up-regulating ANKRD13A, which might induce the immune escape of AML cells. ChIP analysis revealed that the regulatory effects of USP30-AS1 on USP30 and ANKRD13A are associated with H3K4me3 and H3K27Ac. In summary, USP30-AS1 probably promotes AML cell survival by cis-regulating USP30 and ANKRD13A.

Indexed as

CarcinogenesisCell Line, TumorCell SurvivalGene Expression Regulation, NeoplasticHumansLeukemia, Myeloid, AcuteMembrane ProteinsMitochondrial ProteinsPrognosisRNA, Long NoncodingThiolester HydrolasesANKRD13A protein, humanMembrane ProteinsMitochondrial ProteinsRNA, Long NoncodingThiolester HydrolasesUsp30 protein, humanAcute myeloid leukemiaANKRD13AMethylationUSP30USP30-AS1

Identifiers

PMID34694569
PMCPMC8732929
OpenAlexW3210294885

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.