Evidence map›Paper›PMID 26175950›Full record

ArticleAmerican journal of cancer research2015

Six1 promotes glioblastoma cell proliferation and invasion by upregulation of connective tissue growth factor.

Tian Tian, Aimin Li, Hong Lu, Ran Luo, Mingzhi Zhang, Zhaoming Li

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-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

13 citing papers in PubMed, 22 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

6 authors at 2 institutions in 1 country.

Tian TianDepartment of Neurology, The First Affiliated Hospital, Zhengzhou University Zhengzhou 450052, People's Republic of China ; Institute of Clinical Medicine, The First Affiliated Hospital, Zhengzhou University Zhengzhou 450052, People's Republic of China.
Aimin LiDepartment of Oncology, The First Affiliated Hospital, Zhengzhou University Zhengzhou 450052, People's Republic of China.
Hong LuDepartment of Neurology, The First Affiliated Hospital, Zhengzhou University Zhengzhou 450052, People's Republic of China ; Institute of Clinical Medicine, The First Affiliated Hospital, Zhengzhou University Zhengzhou 450052, People's Republic of China.
Ran LuoDepartment of Neurosurgery, Yichang Central People's Hospital and The First Affiliated Hospital of China Three Gorges University 443002 People's Republic of China.
Mingzhi ZhangDepartment of Oncology, The First Affiliated Hospital, Zhengzhou University Zhengzhou 450052, People's Republic of China.
Zhaoming LiDepartment of Oncology, The First Affiliated Hospital, Zhengzhou University Zhengzhou 450052, People's Republic of China ; Institute of Clinical Medicine, The First Affiliated Hospital, Zhengzhou University Zhengzhou 450052, People's Republic of China.
First Affiliated Hospital of Zhengzhou University · CNYichang Central People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is the deadliest and most common form of malignant primary brain tumor in humans. However, until now, little is known about the glioma genesis and progression at the molecular level. Here we report that overexpression of sine oculis homeobox homolog 1 (Six1), a developmental transcription factor implicated in tumor onset and progression, can significantly promote glioblastoma cell proliferation and invasion by upregulating connective tissue growth factor (CTGF). Our results revealed that expression of Six1 mRNA was increased and small hairpin RNAi silencing of Six1 could dramatically inhibit cell proliferation and invasion in GBM. Moreover, it was found that CTGF gene could be transcriptionally regulated by Six1. Its overexpression induced CTGF up-regulation in GBM at both the mRNA and protein level, and significantly enhanced the activity of CTGF promoter in these tumor cells, while decreasing CTGF expression impeded Six1-induced cell proliferation and invasion, revealing that CTGF is required for Six1-mediated GBM growth and metastasis. Collectively, these findings suggest that Six1 overexpression may contribute to cell proliferation and invasion via upregulation of CTGF in GBM. Our study provides new insights into the important roles of Six1 and CTGF in tumor regulation, suggesting that Six1 might be a potential therapeutic target for preventing proliferation and metastasis of GBM.

Indexed as

cell proliferationCTGFglioblastomainvasionSix1

Identifiers

PMID26175950
PMCPMC4497448
OpenAlexW2409290408

What OpenQuestion holds

Textmetadata
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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.