Evidence map›Paper›PMID 27240802›Full record

ArticleCell biology and toxicology2016

Silencing GTSE-1 expression inhibits proliferation and invasion of hepatocellular carcinoma cells.

Lei Guo, Shumin Zhang, Bo Zhang, Wanyong Chen, Xiaoqiang Li, Wentao Zhang, Chenhao Zhou, Jubo Zhang, Ning Ren, Qinghai Ye

Open access · hybridAbstract read
In one paragraph

Article in Cell biology and toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. GTSE1-driven ZEB1 stabilization promotes pulmonary fibrosis through the epithelial-to-mesenchymal transition.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. ESPL1 is Elevated in Hepatocellular Carcinoma and Predicts Prognosis.International journal of general medicine · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. LncRNAAnnals of translational medicine · 2021
    Article
  16. GTSE1 promotes prostate cancer cell proliferation via the SP1/FOXM1 signaling pathway.Laboratory investigation; a journal of technical methods and pathology · 2021
    Article
  17. Article
  18. Article
  19. Article
  20. Article
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

10 authors at 4 institutions in 1 country.

Lei GuoLiver Cancer Institute and Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Shumin ZhangDepartment of Radiation Oncology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Bo ZhangLiver Cancer Institute and Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Wanyong ChenLiver Cancer Institute and Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Xiaoqiang LiLiver Cancer Institute and Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Wentao ZhangLiver Cancer Institute and Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Chenhao ZhouLiver Cancer Institute and Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Jubo ZhangLiver Cancer Institute and Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Ning RenLiver Cancer Institute and Zhongshan Hospital, Fudan University, Shanghai, 200032, China. ren.ning@zs-hospital.sh.cn.
Qinghai YeLiver Cancer Institute and Zhongshan Hospital, Fudan University, Shanghai, 200032, China. ye.qinghai@zs-hospital.sh.cn.
Fudan University · CNMinistry of Education of the People's Republic of China · CNZhongshan Hospital · CNThe First Affiliated Hospital, Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

G2 and S phase-expressed-1 (GTSE1) was recently reported to upregulate in several types of human cancer, based on negatively regulate p53 expression. However, its expression and functional roles in hepatocellular carcinoma (HCC) remain unknown. In this study, GTSE1 was observed to be highly expressed in HCC specimens and cell lines both at messenger RNA (mRNA) and protein levels. Furthermore, high GTSE1 expression was positively associated with tumor size, venous invasion, advanced tumor stage, and short overall survival. Moreover, we generated stable GTSE1 knockdown HCC cell lines to explore the effects of GTSE1 silencing on the growth and invasion of HCC in vitro. In determining the pathway through which GTSE1 regulated cell proliferation and invasion, GTSE1 silencing was found to inhibit AKT phosphorylation and downregulated cell cycle-related protein. In addition, GTSE1 downregulation decreased the growth of xenografts. In conclusion, these results indicated for the first time that overexpression of GTSE1 was involved in the progress of HCC, enhancing proliferation and promoting cell invasion in HCC cells.

Indexed as

AnimalsCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHeterograftsHumansLiver NeoplasmsMaleMiceMice, Inbred BALB CMicrotubule-Associated ProteinsPhosphorylationProto-Oncogene Proteins c-aktRNA, MessengerGTSE1 protein, humanMicrotubule-Associated ProteinsProto-Oncogene Proteins c-aktRNA, MessengerGTSE1HCCInvasionPrognosisProliferation

Identifiers

PMID27240802
PMCPMC4945688
OpenAlexW2409436219

What OpenQuestion holds

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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.