Evidence map›Paper›PMID 28287612›Full record

ArticleOncogenesis2017

Overexpression of SMC4 activates TGFβ/Smad signaling and promotes aggressive phenotype in glioma cells.

L Jiang, J Zhou, D Zhong, Y Zhou, W Zhang, W Wu, Z Zhao, W Wang, W Xu, L He and 4 more

Erratum issuedAbstract read
In one paragraph

Article in Oncogenesis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
–field-weighted citation impact
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.

  1. Article
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  5. SMC4 Promotes Prostate Cancer Cell Proliferation and Metastasis via the Rheb/mTOR Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Identification of SMC2 and SMC4 as prognostic markers in breast cancer through bioinformatics analysis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Association ofAging · 2023
    Article
  15. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors.

L JiangKey Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences; Affiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, China.
J ZhouGuangdong Province Key Laboratory of Brain Function and Disease, Department of Biochemistry, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.
D ZhongNeurosurgical Research Institute, The First Affiliated Hospital of Guangdong Pharmaceutics University, Guangzhou, China.
Y ZhouNeurosurgical Research Institute, The First Affiliated Hospital of Guangdong Pharmaceutics University, Guangzhou, China.
W ZhangDepartment of Pathology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
W WuDepartment of Neurosurgery, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Z ZhaoNeurosurgical Research Institute, The First Affiliated Hospital of Guangdong Pharmaceutics University, Guangzhou, China.
W WangNeurosurgical Research Institute, The First Affiliated Hospital of Guangdong Pharmaceutics University, Guangzhou, China.
W XuNeurosurgical Research Institute, The First Affiliated Hospital of Guangdong Pharmaceutics University, Guangzhou, China.
L HeNeurosurgical Research Institute, The First Affiliated Hospital of Guangdong Pharmaceutics University, Guangzhou, China.
Y MaNeurosurgical Research Institute, The First Affiliated Hospital of Guangdong Pharmaceutics University, Guangzhou, China.
Y HuNeurosurgical Research Institute, The First Affiliated Hospital of Guangdong Pharmaceutics University, Guangzhou, China.
W ZhangNeurosurgical Research Institute, The First Affiliated Hospital of Guangdong Pharmaceutics University, Guangzhou, China.
J LiDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overexpression of structural maintenance of chromosomes 4 (SMC4) has been reported to be involved in tumor cell growth, migration and invasion, and to be correlated with poor prognosis of cancer patient. However, its clinical significance and biological role in glioma remain unknown. Herein, we found that SMC4 expression at both mRNA and protein level was markedly increased in glioma cells and clinical tissues and that it correlated with poor prognosis. SMC4 overexpression markedly promoted the glioma cell proliferation rate and migration and invasive capability in vitro and in vivo, whereas SMC4 downregulation reduced it. Moreover, the transforming growth factor β (TGFβ)/Smad signaling pathway, which was activated in SMC4-transduced glioma cells and inhibited in SMC4-silenced glioma cells, contributed to SMC4-mediated glioma cell aggressiveness. Our results provide new insight into the oncofunction of SMC4 and the mechanism by which the TGFβ/Smad pathway is hyperactivated in gliomas, indicating that SMC4 is a valuable prognostic factor and a potential therapeutic target in gliomas.

Identifiers

PMID28287612
PMCPMC5533949

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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.