Evidence map›Paper›PMID 28748856›Full record

ArticleChinese medical journal2017

The Short Isoform of Nuclear Mitotic Apparatus Protein 1 Functions as a Putative Tumor Suppressor.

Wang-Sen Qin, Jin Wu, Yang Chen, Fa-Cai Cui, Fu-Ming Zhang, Guan-Ting Lyu, Hong-Mei Zhang

Open access · goldAbstract read
In one paragraph

Article in Chinese medical journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.1field-weighted citation impact, top 49% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Observational
  4. 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 4 institutions in 1 country.

Wang-Sen QinDepartment of Clinical Laboratory, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, China.
Jin WuDepartment of Clinical Oncology, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 710032, China.
Yang ChenCentral Laboratory, Haikou People's Hospital, Haikou, Hainan 570208, China.
Fa-Cai CuiDepartment of Clinical Laboratory, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, China.
Fu-Ming ZhangDepartment of Clinical Laboratory, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, China.
Guan-Ting LyuDepartment of Blood Transfusion, Tangdu Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 710032, China.
Hong-Mei ZhangDepartment of Clinical Oncology, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 710032, China.
Henan Provincial People's Hospital · CNXijing Hospital · CNAir Force Medical University · CNHaikou City People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNuclear mitotic apparatus protein 1 (NuMA1) had been reported to produce three groups of isoforms categorized as long, middle, and short groups, of which short NuMA displayed distinct localization patterns compared to long and middle isoforms. However, the function of short NuMA was not clear in the progress of cancer formation. This study aimed to unveil the role of short NuMA in cancer pathogenesis.

methodsThe expression levels of short isoforms were explored in paired gastric carcinoma (GC) samples and different cell lines. Furthermore, the short isoform behaved as a putative tumor suppressor based on cell proliferation and cell colony formation assays. Pull-down assay and whole-genome gene expression analysis were carried out to search candidate interaction partners of short NuMA.

resultsThe expression of short NuMA was highly expressed in S and G2 phases of the cell cycle; compared with nontumor tissues, short NuMA downregulated in nine GCs (GC1 [0.131, P = 5 × 10-4]; GC2 [0.316, P = 3 × 10-5]; GC3 [0.111, P = 6 × 10-4]; GC4 [0.456, P = 0.011]; GC5 [0.474, P = 0.001]; GC6 [0.311, P = 0.004]; GC7 [0.28, P = 3 × 10-5]; GC8 [0.298, P = 0.007]; and GC9 [0.344, P = 0.002]). Besides, high expression of short NuMA significantly inhibits cell growth (2.43 × 105 vs. 2.97 × 105, P = 0.0029) and cell clone information in vitro (70 vs. 2, P = 1.67 × 10-45). Short NuMA could bind with alpha-actinin-4 (ACTN4), a putative tumor promoting gene. Overexpression of short NuMA could tremendously decrease the expression of MYB proto-oncogene like 2 (MYBL2) of about 92-fold, which played an important role in the cell cycles.

conclusionsShort isoform of NuMA might be functioned as a putative role of tumor suppressor. Further studies should be made to illuminate the relationship between ACTN4, MYBL2, and tumor progression.

Indexed as

ActininAgedAntigens, NuclearCell CycleCell Cycle ProteinsCell LineCell ProliferationHeLa CellsHumansMaleMiddle AgedNuclear Matrix-Associated ProteinsProtein IsoformsProto-Oncogene MasTrans-ActivatorsActininACTN4 protein, humanAntigens, NuclearCell Cycle ProteinsMAS1 protein, humanMYBL2 protein, humanNuclear Matrix-Associated ProteinsNUMA1 protein, humanProtein IsoformsProto-Oncogene MasTrans-Activators

Identifiers

PMID28748856
PMCPMC5547835
OpenAlexW2741025694

What OpenQuestion holds

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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.