Evidence map›Paper›PMID 30082910›Full record

ArticleOncogene2019

Hypermethylated gene ANKDD1A is a candidate tumor suppressor that interacts with FIH1 and decreases HIF1α stability to inhibit cell autophagy in the glioblastoma multiforme hypoxia microenvironment.

Jianbo Feng, Yan Zhang, Xiaoling She, Yingnan Sun, Li Fan, Xing Ren, Haijuan Fu, Changhong Liu, Peiyao Li, Chunhua Zhao and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

32 citing papers in PubMed, 42 citations in OpenAlex.

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  20. Unfolding the role of autophagy in the cancer metabolism.Biochemistry and biophysics reports · 2021
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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

14 authors at 6 institutions in 3 countries.

Jianbo FengHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, 410013, Hunan, China.
Yan ZhangHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, 410013, Hunan, China.
Xiaoling SheThe Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China.
Yingnan SunHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, 410013, Hunan, China.
Li FanDepartment of Biochemistry, University of California, Riverside, CA, 92521, USA.
Xing RenHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, 410013, Hunan, China.
Haijuan FuHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, 410013, Hunan, China.
Changhong LiuHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, 410013, Hunan, China.
Peiyao LiHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, 410013, Hunan, China.
Chunhua ZhaoHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, 410013, Hunan, China.
Qiang LiuThe Third Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China.
Qing LiuThe Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Guiyuan LiHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, 410013, Hunan, China.
Minghua WuHunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, 410013, Hunan, China. wuminghua554@aliyun.com.
Central South University · CNMinistry of Health · UGHunan Cancer Hospital · CNSecond Xiangya Hospital of Central South University · CNUniversity of California, Riverside · USXiangya Hospital Central South University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81272297
6 · The paper itself

Abstract

Ectopic epigenetic mechanisms play important roles in facilitating tumorigenesis. Here, we first demonstrated that ANKDD1A is a functional tumor suppressor gene, especially in the hypoxia microenvironment. ANKDD1A directly interacts with FIH1 and inhibits the transcriptional activity of HIF1α by upregulating FIH1. In addition, ANKDD1A decreases the half-life of HIF1α by upregulating FIH1, decreases glucose uptake and lactate production, inhibits glioblastoma multiforme (GBM) autophagy, and induces apoptosis in GBM cells under hypoxia. Moreover, ANKDD1A is highly frequently methylated in GBM. The tumor-specific methylation of ANKDD1A indicates that it could be used as a potential epigenetic biomarker as well as a possible therapeutic target.

Indexed as

AutophagyDNA MethylationTumor HypoxiaAnkyrin RepeatApoptosisCell Line, TumorChromosomes, Human, Pair 15Gene Expression Regulation, NeoplasticGenes, Tumor SuppressorGlioblastomaGlucoseHalf-LifeHumansHypoxia-Inducible Factor 1, alpha SubunitIntracellular Signaling Peptides and ProteinsLactatesANKDD1A protein, humanGlucoseHIF1AN protein, humanHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitIntracellular Signaling Peptides and ProteinsLactatesMixed Function OxygenasesNeoplasm ProteinsRecombinant ProteinsRepressor ProteinsTumor Suppressor ProteinsVHL protein, humanVon Hippel-Lindau Tumor Suppressor Protein

Identifiers

PMID30082910
PMCPMC6318269
OpenAlexW2887920237

What OpenQuestion holds

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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.