Evidence map›Paper›PMID 38863009›Full record

ArticleBiology direct2024

Hypoxia-induced activation of HIF-1alpha/IL-1beta axis in microglia promotes glioma progression via NF-κB-mediated upregulation of heparanase expression.

Jinchao Si, Jingya Guo, Xu Zhang, Wei Li, Shen Zhang, Shuyu Shang, Quanwu Zhang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biology direct, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Article
  2. Article
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  4. Acidosis, Iron Dyshomeostasis and Inflammatory Injury.International journal of molecular sciences · 2026
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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

7 authors.

Jinchao SiDepartment of Neurology, the Second Affiliated Hospital of Zhengzhou University, Zhengzhou, 450014, China.
Jingya GuoDepartment of Neuroelectrophysiology, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou, 450007, China.
Xu ZhangDepartment of General Practice, the Second Affiliated Hospital of Zhengzhou University, Zhengzhou, 450014, China.
Wei LiDepartment of Physiology, School of Basic Medicine, Zhengzhou University, Zhengzhou, 450066, China.
Shen ZhangDepartment of Neuroelectrophysiology, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou, 450007, China.
Shuyu ShangDepartment of Physiology, Medical College, HuangHe Science and Technology University, Zhengzhou, 450064, China.
Quanwu ZhangDepartment of Pathology, Zhengzhou Central Hospital Affiliated to Zhengzhou University, No. 16 Tongbai North Road, Zhengzhou, Henan Province, 450007, China. sahzjk@zzu.edu.cn.

Funding

the Health Commission of Henan Province LHGJ20210387
6 · The paper itself

Abstract

backgroundGlioma is a common tumor that occurs in the brain and spinal cord. Hypoxia is a crucial feature of the tumor microenvironment. Tumor-associated macrophages/microglia play a crucial role in the advancement of glioma. This study aims to illuminate the detailed mechanisms by which hypoxia regulates microglia and, consequently, influences the progression of glioma.

methodsThe glioma cell viability and proliferation were analyzed by cell counting kit-8 assay and 5-ethynyl-2'-deoxyuridine assay. Wound healing assay and transwell assay were implemented to detect glioma cell migration and invasion, respectively. Enzyme-linked immunosorbent assay was conducted to detect protein levels in cell culture medium. The protein levels in glioma cells and tumor tissues were evaluated using western blot analysis. The histological morphology of tumor tissue was determined by hematoxylin-eosin staining. The protein expression in tumor tissues was determined using immunohistochemistry. Human glioma xenograft in nude mice was employed to test the influence of hypoxic microglia-derived interleukin-1beta (IL-1β) and heparanase (HPSE) on glioma growth in vivo.

resultsHypoxic HMC3 cells promoted proliferation, migration, and invasion abilities of U251 and U87 cells by secreting IL-1β, which was upregulated by hypoxia-induced activation of hypoxia inducible factor-1alpha (HIF-1α). Besides, IL-1β from HMC3 cells promoted glioma progression and caused activation of nuclear factor-κB (NF-κB) and upregulation of HPSE in vivo. We also confirmed that IL-1β facilitated HPSE expression in U251 and U87 cells by activating NF-κB. Hypoxic HMC3 cells-secreted IL-1β facilitated the proliferation, migration, and invasion of U251 and U87 cells via NF-κB-mediated upregulation of HPSE expression. Finally, we revealed that silencing HPSE curbed the proliferation and metastasis of glioma in mice.

conclusionHypoxia-induced activation of HIF-1α/IL-1β axis in microglia promoted glioma progression via NF-κB-mediated upregulation of HPSE expression.

Indexed as

GliomaGlucuronidaseHypoxia-Inducible Factor 1, alpha SubunitInterleukin-1betaMice, NudeMicrogliaNF-kappa BUp-RegulationAnimalsBrain NeoplasmsCell Line, TumorCell MovementCell ProliferationDisease ProgressionHeparanaseHumansGlucuronidaseHeparanaseHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitIL1B protein, humanInterleukin-1betaNF-kappa BGliomaHeparanaseHypoxiaHypoxia inducible factor-1αInterleukin-1βMicroglia

Identifiers

PMID38863009
PMCPMC11165725

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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.