Evidence map›Paper›PMID 25428991›Full record

ArticleMolecular biology of the cell2015

Transcriptional factor specificity protein 1 (SP1) promotes the proliferation of glioma cells by up-regulating midkine (MDK).

Jingyan Luo, Xiaoxiao Wang, Zhibo Xia, Lixuan Yang, Zhiming Ding, Shiyuan Chen, Bingquan Lai, Nu Zhang

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

45 citing papers in PubMed, 73 citations in OpenAlex.

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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 2 countries.

Jingyan LuoForevergen Biosciences Center, R&D Unit 602, Guangzhou 510000, China Department of Neurosurgery, First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China.
Xiaoxiao WangDepartment of Medical Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, and Collaborative Innovation Center for Cancer Medicine, Guangzhou, 510060, China.
Zhibo XiaDepartment of Neurosurgery, First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China.
Lixuan YangDepartment of Neurosurgery, First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China.
Zhiming DingDepartment of Neurosurgery, Huang Pu Division, First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510000, China.
Shiyuan ChenDepartment of Neurology and Northwestern Brain Tumor Institute, Center of Genetic Medicine, Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL 60611.
Bingquan LaiForevergen Biosciences Center, R&D Unit 602, Guangzhou 510000, China lbq@forevergen.cn zhangnu1008@163.com.
Nu ZhangDepartment of Neurosurgery, First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China lbq@forevergen.cn zhangnu1008@163.com.
Sun Yat-sen University · CNNorthwestern University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Midkine (MDK) expression is associated with the proliferation of many cancers, including glioma. However, the upstream signaling that leads to MDK accumulation remains elusive. This study investigates the molecular mechanism that induces MDK overexpression in human glioma. The Repository for Molecular Brain Neoplasia Data was analyzed to identify potential MDK regulators. Expression of MDK and specificity protein 1 (SP1) was compared in glioma specimens. Chromatin immunoprecipitation assay was used to confirm the transcriptional regulation. MDK-force-expressed, SP1-silenced glioma cells were used to test rescue effects in vitro and in vivo. MDK and SP1 expression in gliomas was significantly higher than in adjacent tissues and was positively correlated in glioma clinical samples and cell lines. The promoter of the human MDK gene has a putative SP1 binding site. SP1 binds to the promoter of the MDK gene and directly regulates MDK expression. MDK or SP1 gene silencing inhibited the proliferation of glioma cells and reduced the tumor volume in nude mice. Overexpression of MDK in SP1-silenced cells could partially rescue the SP1 inhibition effects in vivo and in vitro. SP1 directly up-regulated the expression of MDK, and the SP1-MDK axis cooperated in glioma tumorigenesis.

Indexed as

Gene Expression Regulation, NeoplasticTranscriptional ActivationAnimalsCell Line, TumorCell ProliferationGliomaHumansMiceMice, NudeMidkineNerve Growth FactorsPromoter Regions, GeneticSp1 Transcription FactorUp-RegulationMDK protein, humanMidkineNerve Growth FactorsSP1 protein, humanSp1 Transcription Factor

Identifiers

PMID25428991
PMCPMC4310735
OpenAlexW2315542372

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.