Evidence map›Paper›PMID 34888748›Full record

ArticleIn vitro cellular & developmental biology. Animal2021

Nucleoporin 37 promotes the cell proliferation, migration, and invasion of gastric cancer through activating the PI3K/AKT/mTOR signaling pathway.

Jishui Zhang, Wenhao Lv, Yagang Liu, Weihua Fu, Baosheng Chen, Qiutong Ma, Xin Gao, Xiuxia Cui

Abstract read
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In one paragraph

Article in In vitro cellular & developmental biology. Animal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. Advances in the understanding of nuclear pore complexes in human diseases.Journal of cancer research and clinical oncology · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. 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.

Jishui ZhangThe Second Department of General Surgery, Cangzhou Central Hospital, No. 16 Xinhua West Road, Cangzhou, 061001, Hebei, China. jishui_z1980@163.com.
Wenhao LvThe Second Department of General Surgery, Cangzhou Central Hospital, No. 16 Xinhua West Road, Cangzhou, 061001, Hebei, China.
Yagang LiuThe Second Department of General Surgery, Cangzhou Central Hospital, No. 16 Xinhua West Road, Cangzhou, 061001, Hebei, China.
Weihua FuDepartment of General Surgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Baosheng ChenThe Second Department of General Surgery, Cangzhou Central Hospital, No. 16 Xinhua West Road, Cangzhou, 061001, Hebei, China.
Qiutong MaThe Second Department of General Surgery, Cangzhou Central Hospital, No. 16 Xinhua West Road, Cangzhou, 061001, Hebei, China.
Xin GaoDepartment of Radiotherapy, Cangzhou Central Hospital, Cangzhou, 061001, Hebei, China.
Xiuxia CuiDepartment of Nuclear Medicine, Cangzhou Central Hospital, Cangzhou, 061001, Hebei, China.
Cangzhou Central Hospital · CNTianjin Medical University General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer is a kind of malignant tumor in the world. Emerging studies have proved the regulatory role of nucleoporin 37 in the development of several malignant tumors. However, the potential effect of NUP37 in gastric cancer is still unclear. In this study, we searched for the Cancer Genome Atlas analysis to explore the potential correlation between NUP37 and gastric cancer. Then, we analyzed NUP37 expression in gastric cancer tissues and cell lines. After constructing a NUP37-silenced model in NCI-N87 cells and a NUP37-overexpressed model in MKN45 cells, we evaluated the role of NUP37 in cell proliferation, migration, and invasion as well as its underlying mechanism. TCGA analysis showed that NUP37 expression was highly expressed in stomach adenocarcinoma, which showed a lower survival rate than normal samples. Moreover, NUP37 was found to be highly expressed in gastric cancer tissues and cell lines. Functionally, NUP37 deficiency promoted gastric cancer cell apoptosis and inhibited cell proliferation, migration, and invasion, whereas NUP37 overexpression exhibited the opposite results. Mechanically, upregulation of NUP37 activated the PI3K/AKT/mTOR signaling pathway. Furthermore, the rescue assay exhibited that the mTOR inhibitor rapamycin significantly reversed the promoting effect of NUP37 in cell proliferation, migration, and invasion. In conclusion, our study identified that NUP37 promoted malignant behavior of gastric cancer cells including invasion, proliferation, and migration through activating the PI3K and its downregulated signaling pathway, indicating that NUP37 might become a novel prognostic target for further gastric cancer therapy.

Indexed as

Nuclear Pore Complex ProteinsStomach NeoplasmsAdenocarcinomaApoptosisCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesMTOR protein, humanNuclear Pore Complex ProteinsNUP37 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAKTGastric cancermTORNUP37PI3K

Identifiers

PMID34888748
OpenAlexW4200586818

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.