Evidence map›Paper›PMID 32029898›Full record

ArticleOncogene2020

Bclaf1 is a direct target of HIF-1 and critically regulates the stability of HIF-1α under hypoxia.

Anwen Shao, Yue Lang, Mengdong Wang, Chao Qin, Yu Kuang, Yide Mei, Degui Lin, Shuo Zhang, Jun Tang

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 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
1.0field-weighted citation impact, top 28% 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, 24 citations in OpenAlex.

  1. Article
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  6. Review
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  11. Article
  12. Article
  13. Review
  14. Article
  15. Function of BCLAF1 in human disease.Oncology letters · 2022
    Review
  16. Article
  17. Review
  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

9 authors at 2 institutions in 1 country.

Anwen Shao *Department of Basic Veterinary Medicine, College of Veterinary Medicine, China Agricultural University, Beijing, 100193, China.
Yue Lang *Department of Basic Veterinary Medicine, College of Veterinary Medicine, China Agricultural University, Beijing, 100193, China.
Mengdong WangDepartment of Basic Veterinary Medicine, College of Veterinary Medicine, China Agricultural University, Beijing, 100193, China.
Chao QinDepartment of Basic Veterinary Medicine, College of Veterinary Medicine, China Agricultural University, Beijing, 100193, China.
Yu KuangDepartment of Basic Veterinary Medicine, College of Veterinary Medicine, China Agricultural University, Beijing, 100193, China.
Yide MeiSchool of Life Sciences, University of Science and Technology of China, Hefei, 230026, Anhui, China.
Degui LinDepartment of Clinic Veterinary Medicine, College of Veterinary Medicine, China Agricultural University, Beijing, 100193, China.
Shuo ZhangDepartment of Clinic Veterinary Medicine, College of Veterinary Medicine, China Agricultural University, Beijing, 100193, China.
Jun TangDepartment of Basic Veterinary Medicine, College of Veterinary Medicine, China Agricultural University, Beijing, 100193, China. jtang@cau.edu.cn.
China Agricultural University · CNUniversity of Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxic stress is intimately connected with tumor progression, with hypoxia-inducible factor-1α (HIF-1α) being a critical regulator in this process. HIF-1α is stabilized in response to hypoxia, which is required for the induction of gene transcriptions important for hypoxic adaptation. Bclaf1 is a multifunctional protein involved in tumorigenesis, however, its role in this process is not well characterized. Here we report Bclaf1 is a direct transcriptional target of HIF-1 and upregulated in multiple cell lines during hypoxia. Importantly, we found Bclaf1 is involved in the stabilization of HIF-1α during long-term hypoxic treatments. Compared with the control cells, the protein level and stability of HIF-1α in Bclaf1 knockdown or knockout cells is greatly compromised after long-term hypoxic treatments, concomitant with the impaired inductions of HIF-1 target gene transcription. Bclaf1 knockout HeLa cells exhibit a reduced tumor growth in mice xenografts, in which the expressions of HIF-1α and its target genes are also decreased. Bclaf1 binds to HIF-1α in the nucleus, and this interaction is required for Bclaf1 to stabilize HIF-1α in hypoxic condition. These results uncover a positive feedback loop, HIF-1-Bclaf1, that sustains HIF-1 activity during long-term hypoxic conditions by binding to and protecting HIF-1α from degradation, and suggest that Bclaf1 may promote tumor progression by enhancing HIF-1α stability.

Indexed as

Feedback, PhysiologicalGene Expression Regulation, NeoplasticAnimalsCell HypoxiaCell Line, TumorDisease ProgressionFemaleGene Knockdown TechniquesGene Knockout TechniquesHumansHypoxia-Inducible Factor 1, alpha SubunitMiceNeoplasmsProtein StabilityRepressor ProteinsTranscription, GeneticBCLAF1 protein, humanHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitRepressor ProteinsTumor Suppressor Proteins

Identifiers

PMID32029898
OpenAlexW3004642658

What OpenQuestion holds

Textmetadata
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.