Evidence map›Paper›PMID 33742130›Full record

ReviewCancer gene therapy2022

Glioma pathogenesis-related protein 1 performs dual functions in tumor cells.

Junjie Wang, Zeyu Li, Fenfen Yin, Rui Zhang, Ying Zhang, Zhengxin Wang, Xiumei Sheng

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cancer gene therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. CAP superfamily proteins in human: a new target for cancer therapy.Medical oncology (Northwood, London, England) · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. 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

7 authors at 2 institutions in 2 countries.

Junjie WangDepartment of Pathophysiology, Jiangsu University School of Medicine, Zhenjiang, 212013, Jiangsu, China.
Zeyu LiDepartment of Biochemistry and Molecular Biology, Jiangsu University School of Medicine, Zhenjiang, 212013, Jiangsu, China.
Fenfen YinDepartment of Biochemistry and Molecular Biology, Jiangsu University School of Medicine, Zhenjiang, 212013, Jiangsu, China.
Rui ZhangDepartment of Biochemistry and Molecular Biology, Jiangsu University School of Medicine, Zhenjiang, 212013, Jiangsu, China.ORCID http://orcid.org/0000-0002-6398-0355
Ying ZhangDepartment of Biochemistry and Molecular Biology, Jiangsu University School of Medicine, Zhenjiang, 212013, Jiangsu, China.ORCID http://orcid.org/0000-0002-6505-4822
Zhengxin WangThe Center for Cancer Research and Therapeutic Development, Department of Biological Sciences, Clark Atlanta University, Atlanta, GA, 30314, USA. zwang@cau.edu.ORCID http://orcid.org/0000-0002-7721-7326
Xiumei ShengDepartment of Biochemistry and Molecular Biology, Jiangsu University School of Medicine, Zhenjiang, 212013, Jiangsu, China. shengxiumei@ujs.edu.cn.ORCID http://orcid.org/0000-0002-9716-0195
Jiangsu University · CNCenter for Cancer Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioma pathogenesis-related protein 1 (GLIPR1) was identified as an oncoprotein in some cancer types including gliomas, breast cancers, melanoma cancers, and Wilms tumors, but as a tumor suppressor in some other types of cancers, such as prostate cancers, lung cancers, bladder cancers, and thyroid cancers. In gliomas, GLIPR1 promotes the migration and invasion of glioma cells by interaction with the actin polymerization regulator Neural Wiskott-Aldrich syndrome protein (N-WASP) and then abolishes the negative effects of Heterogeneous nuclear ribonuclear protein K (hnRNPK). In prostate cancers, high levels of GLIPR1 induce apoptosis and destruction of oncoproteins. In lung cancers, overexpression of GLIPR1 inhibits the growth of lung cancer cells partially through inhibiting the V-ErbB avian erythroblastic leukemia viral oncogene homolog3 (ErbB3) pathway. However, the mechanisms that GLIPR1 performs its function in other tumors still remain unclear. The tumor suppressing role of GLIPR1 has been explored to the cancer treatment. The adenoviral vector-mediated Glipr1 (AdGlipr1) gene therapy and the GLIPR1-transmembrane domain deleted (GLIPR1-ΔTM) protein therapy both showed antitumor activities and stimulated immune response in prostate cancers. Whether GLPIR1 can be used to treat other tumors is an important topic to be explored. Among which, whether GLPIR1 can be used to treat lung cancer by atomizing inhalation is the key topic we care about. If it does, this therapy has a wide application prospect and is a great progression in lung cancer treatment.

Indexed as

GliomaLung NeoplasmsProstatic NeoplasmsHumansMaleMembrane ProteinsNeoplasm ProteinsNerve Tissue ProteinsNuclear ProteinsGLIPR1 protein, humanMembrane ProteinsNeoplasm ProteinsNerve Tissue ProteinsNuclear Proteins

Identifiers

PMID33742130
OpenAlexW3138915752

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.