Evidence map›Paper›PMID 30613163›Full record

ArticleCancer management and research2019

Knockdown of nucleophosmin 1 suppresses proliferation of triple-negative breast cancer cells through activating CDH1/Skp2/p27kip1 pathway.

De Zeng, Yingsheng Xiao, Jianling Zhu, Chunyan Peng, Weiquan Liang, Haoyu Lin

Open access · goldAbstract read
In one paragraph

Article in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  11. KPNA2 promotes renal cell carcinoma proliferation and metastasis via NPM.Journal of cellular and molecular medicine · 2021
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  18. Cancer management and research · 2019
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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

6 authors at 3 institutions in 1 country.

De ZengDepartment of Medical Oncology, Cancer Hospital of Shantou University Medical College, Shantou 515031, China, dezeng@stu.edu.cn.
Yingsheng XiaoDepartment of Thyroid Surgery, Shantou Central Hospital, Shantou 515000, China.
Jianling ZhuDepartment of Pathology, Cancer Hospital of Shantou University Medical College, Shantou 515031, China.
Chunyan PengDepartment of Clinical Laboratory, Taihe Hospital of Hubei University of Medicine, Hubei 442008, China.
Weiquan LiangDepartment of Thyroid and Breast Surgery, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515000, China, rainlhy@stu.edu.cn.
Haoyu LinDepartment of Thyroid and Breast Surgery, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515000, China, rainlhy@stu.edu.cn.
Shantou University · CNHubei University of Medicine · CNShantou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNPM1 is a multifunctional phosphoprotein that commutes between the cytoplasm and nucleus in cell cycle process, which appears to be actively involved in tumorigenesis. Herein, we sought to investigate the possible role and prognostic value of NPM1 in triple-negative breast cancer (TNBC).

methodsAn array of public databases, including bc-GenExMiner v4.0, GOBO, GEPIA, UAL-CAN, ONCOMINE database and Kaplan-Meier plotter, were used to investigate the expression feature and potential function of NPM1 in TNBC. Immunohistochemistry, immunofluorescence, proliferation and colony formation, flow cytometry and western-blotting assays were used to analyze and verify the function and relevant mechanism of NPM1 in TNBC tissues and cells.

resultsAccording to analysis from bc-GenExMiner, the expression level of NPM1 was significantly higher in basal-like subtypes than luminal-A, HER-2 or normal-like subtypes of breast cancer (

conclusionsNPM1 is significantly high expressed basal-like/triple-negative breast cancer and is correlated with shorter RFS and OS in this subset of patients. Knockdown of NPM1 impairs the proliferative capacity of TNBC cells via activation of the CDH1/Skp2/p27kip1 pathway. Targeting NPM1 is a potential therapeutic strategy against TNBC.

Indexed as

mechanismnucleophosmin 1prognosisproliferationtriple-negative breast cancer

Identifiers

PMID30613163
PMCPMC6306051
OpenAlexW2904209505

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.