Evidence map›Paper›PMID 29547938›Full record

ArticleNeuro-oncology2018

Cancer-testis specific gene OIP5: a downstream gene of E2F1 that promotes tumorigenesis and metastasis in glioblastoma by stabilizing E2F1 signaling.

Jiang He, Yuzu Zhao, Erhu Zhao, Xianxing Wang, Zhen Dong, Yibiao Chen, Liqun Yang, Hongjuan Cui

Open access · bronzeAbstract read
In one paragraph

Article in Neuro-oncology, 2018. 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
1.5field-weighted citation impact, top 18% 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, 42 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. E2F1-induced upregulation ofHistology and histopathology · 2025
    Article
  4. Review
  5. Review
  6. Article
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  10. The mitosis-related geneAnnals of translational medicine · 2023
    Article
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  12. Article
  13. Frontiers in immunology · 2022
    Article
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  15. Review
  16. Article
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  19. Article
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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

8 authors at 2 institutions in 1 country.

Jiang HeState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.
Yuzu ZhaoState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.
Erhu ZhaoState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.
Xianxing WangState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.
Zhen DongState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.
Yibiao ChenState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.
Liqun YangState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.
Hongjuan CuiState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.
Southwest University · CNState Key Laboratory of Silkworm Genomic Biology

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The cancer-testis specific gene Opa interacting protein 5 (OIP5) is reactivated in many human cancers, but its functions in glioblastoma remain unclear. Here, we assessed the significance of OIP5 in the tumorigenesis and metastasis of glioblastoma for the first time. Methods: An immunohistochemistry assay was performed to detect OIP5 expression changes in glioblastoma patients. Overall survival analysis was performed to evaluate the prognostic significance of OIP5. Growth curve, colony formation, and transwell assays were used to analyze cell proliferation and metastasis. Tumorigenicity potential was investigated in orthotopic tumor models, and immunoprecipitation, chromatin immunoprecipitation, and luciferase assays were employed to explore the mechanisms underlying the activation of OIP5 expression by E2F transcription factor 1 (E2F1) to stabilize and maintain E2F1 signaling. Results: OIP5 was found to be upregulated in glioblastoma patients and to impair patient survival, and the increased expression of OIP5 was positively correlated with tumor stage. Compared with short hairpin green fluorescent protein cells, cells in which OIP5 was knocked down exhibited significantly reduced proliferation, metastasis, colony formation, and tumorigenicity abilities, whereas OIP5 recovery enhanced these abilities. OIP5 was highly correlated with cell cycle progression but had no obvious effects on apoptosis. Notably, we demonstrated a feedback loop in which E2F1 activates the expression of OIP5 to stabilize and maintain E2F1 signaling and promote the E2F1-regulated gene expression that is required for aggressive tumor biology. Conclusions: Collectively, our findings demonstrate that OIP5 promotes glioblastoma progression and metastasis, suggesting that OIP5 is a potential target for anticancer therapy.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBiomarkers, TumorCarcinogenesisCase-Control StudiesCell CycleCell Cycle ProteinsCell MovementCell ProliferationChromosomal Proteins, Non-HistoneE2F1 Transcription FactorGlioblastomaHumansMiceMice, NudeBiomarkers, TumorCell Cycle ProteinsChromosomal Proteins, Non-HistoneE2F1 protein, humanE2F1 Transcription FactorOIP5 protein, human

Identifiers

PMID29547938
PMCPMC6071653
OpenAlexW2790204984

What OpenQuestion holds

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Registered trials

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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.