Evidence map›Paper›PMID 27329597›Full record

ArticleOncotarget2016

Hypoxia upregulates HIG2 expression and contributes to bevacizumab resistance in glioblastoma.

Xing-Gang Mao, Chao Wang, Dong-Ye Liu, Xiang Zhang, Liang Wang, Ming Yan, Wei Zhang, Jun Zhu, Zi-Chao Li, Chen Mi and 6 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  6. Predicting Anticancer Drug Resistance Mediated by Mutations.Pharmaceuticals (Basel, Switzerland) · 2022
    Article
  7. Review
  8. Systematic analysis of potential targets of the curcumin analog pentagamavunon-1 (PGV-1) in overcoming resistance of glioblastoma cells to bevacizumab.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2021
    Article
  9. Article
  10. Endothelial-Tumor Cell Interaction in Brain and CNS Malignancies.International journal of molecular sciences · 2020
    Review
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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

16 authors at 4 institutions in 1 country.

Xing-Gang MaoDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, People's Republic of China.
Chao WangDepartment of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, People's Republic of China.
Dong-Ye LiuNorthern Hospital, General Hospital of PLA Shenyang Military Area Command, Shenyang, Liaoning Province, People's Republic of China.
Xiang ZhangDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, People's Republic of China.
Liang WangDepartment of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, People's Republic of China.
Ming YanDepartment of Orthopaedic Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, People's Republic of China.
Wei ZhangDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, People's Republic of China.
Jun ZhuDepartment of Orthopedics, Changzheng Hospital, Second Military Medical University, Shanghai, People's Republic of China.
Zi-Chao LiDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, People's Republic of China.
Chen MiDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, People's Republic of China.
Jing-Yang TianDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, People's Republic of China.
Guang-Dong HouDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, People's Republic of China.
Si-Yu MiaoDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, People's Republic of China.
Zi-Xuan SongDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, People's Republic of China.
Jin-Cheng LiDepartment of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, People's Republic of China.
Xiao-Yan XueDepartment of Pharmacology, School of Pharmacy, Fourth Military Medical University, Xi'an, Shaanxi Province, People's Republic of China.
Air Force Medical University · CNXijing Hospital · CNGeneral Hospital of Shenyang Military Region · CNSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia contributes to the maintenance of stem-like cells in glioblastoma (GBM), and activates vascular mimicry and tumor resistance to anti-angiogenesis treatments. The present study examined the expression patterns and biological significance of hypoxia-inducible protein 2 (HIG2, also known as HILPDA) in GBM. HIG2 was highly expressed in gliomas and was correlated with tumor grade, and high HIG2 expression independently predicted poor GBM patient prognosis. HIG2 was upregulated during hypoxia and by hypoxia mimics, and HIG2 knockdown in GBM cells inhibited cell proliferation and invasion. HIF1α bound to the HIG2 promoter and increased its expression in GBM cells, and HIG2 upregulated HIF1α expression. Reconstruction of a HIG2-related molecular network using bioinformatics methods revealed that HIG2 is closely correlated with angiogenesis genes, such as VEGFA, in GBM. HIG2 levels positively correlated with VEGFA in GBM samples. In addition, treatment of transplanted xenograft nude mice with bevacizumab (anti-angiogenesis therapy) resulted in HIG2 upregulation at late stages. We conclude that HIG2 is overexpressed in GBM and upregulated by hypoxia, and is a potential novel therapeutic target. HIG2 overexpression is an independent prognostic indicator and may promote tumor resistance to anti-angiogenesis treatments.

Indexed as

Angiogenesis InhibitorsAnimalsAntineoplastic Agents, ImmunologicalBevacizumabBrain NeoplasmsCell HypoxiaCell Line, TumorDrug Resistance, NeoplasmGlioblastomaHumansMiceMice, NudeNeoplasm ProteinsNeovascularization, PathologicUp-RegulationXenograft Model Antitumor AssaysAngiogenesis InhibitorsAntineoplastic Agents, ImmunologicalBevacizumabHILPDA protein, humanNeoplasm Proteinsantiangiogenic therapyglioblastomaHIG2hypoxiaVEGF

Identifiers

PMID27329597
PMCPMC5216980
OpenAlexW2439301799

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.