Evidence map›Paper›PMID 28000106›Full record

ArticleJournal of neuro-oncology2017

Knockdown of NUPR1 inhibits the proliferation of glioblastoma cells via ERK1/2, p38 MAPK and caspase-3.

Jun Li, Siyang Ren, Yongjian Liu, Zhigang Lian, Bin Dong, Yiqun Yao, Yinghui Xu

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of neuro-oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 48 citations in OpenAlex.

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  18. Targeting intrinsically disordered proteins involved in cancer.Cellular and molecular life sciences : CMLS · 2020
    Review
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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

7 authors at 2 institutions in 1 country.

Jun LiDepartment of Neurosurgery, First Affiliated Hospital of Dalian Medical University, 222 Zhong Shan Road, Dalian, 116011, People's Republic of China.
Siyang RenDepartment of Neurosurgery, First Affiliated Hospital of Dalian Medical University, 222 Zhong Shan Road, Dalian, 116011, People's Republic of China.
Yongjian LiuDepartment of Interventional Therapy, First Affiliated Hospital of Dalian Medical University, Dalian, People's Republic of China.
Zhigang LianDepartment of Neurosurgery, First Affiliated Hospital of Dalian Medical University, 222 Zhong Shan Road, Dalian, 116011, People's Republic of China.
Bin DongDepartment of Neurosurgery, First Affiliated Hospital of Dalian Medical University, 222 Zhong Shan Road, Dalian, 116011, People's Republic of China.
Yiqun YaoDepartment of Neurosurgery, First Affiliated Hospital of Dalian Medical University, 222 Zhong Shan Road, Dalian, 116011, People's Republic of China. quince58@163.com.
Yinghui XuDepartment of Neurosurgery, First Affiliated Hospital of Dalian Medical University, 222 Zhong Shan Road, Dalian, 116011, People's Republic of China. xuyh_dl@126.com.
First Affiliated Hospital of Dalian Medical University · CNDalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear protein-1 (NUPR1), located on chromosome 16p11.2, is a stress response factor that plays an important role in the growth and migration of human malignant tumor cells. However, the role of NUPR1 in glioblastoma remains poorly understood. The expression level of NUPR1 was detected by quantitative real-time PCR and immunohistochemistry (IHC). Wound healing, MTT, cell counting and BrdU assays were used to analyze the migration and proliferation of glioblastoma cells after down-regulating NUPR1 expression using a lentiviral vector. FACS analysis and a signaling antibody array kit were used to detect the mechanism by which NUPR1 modulates cell cycle and apoptosis activities in glioblastoma cells. We confirmed that NUPR1 was up-regulated in glioblastoma tissues compared to NB tissues. Down-regulation of NUPR1 suppressed cell migration and proliferation, arrested the cell cycle in the G0/G1 phase and promoted apoptosis in U251 and U87 cells in vitro. Furthermore, the expression levels of phosphorylated ERK1/2, p38 MAPK and cleaved caspase-3 were decreased upon silencing NUPR1 expression in U251 and U87 cells. In summary, NUPR1 plays an important role in the growth and migration of human glioblastoma cells. Knockdown of NUPR1 suppressed glioblastoma cell growth by arresting the cell cycle and inducing cell apoptosis via decreases in the expression of ERK1/2, p38 MAPK and caspase-3.

Indexed as

Caspase 3Cell ProliferationMAP Kinase Signaling SystemApoptosisBasic Helix-Loop-Helix ProteinsCell Cycle CheckpointsCell MovementDown-RegulationFemaleGene Knockdown TechniquesGlioblastomaHumansMaleMiddle AgedNeoplasm ProteinsTumor Cells, CulturedBasic Helix-Loop-Helix ProteinsCaspase 3Neoplasm ProteinsNUPR1 protein, humanApoptosisGloblastomaMigrationNUPR1Proliferation

Identifiers

PMID28000106
OpenAlexW2562421673

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.