Evidence map›Paper›PMID 31819487›Full record

ArticleOncoTargets and therapy2019

Lan Liu, Jing Cao, Jing Zhao, Xiangyu Li, Zhenhe Suo, Huixiang Li

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
6.0field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Review
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  9. Review
  10. Article
  11. Article
  12. Article
  13. The landscape of CRISPR/Cas9 for inborn errors of metabolism.Molecular genetics and metabolism · 2023
    Review
  14. Article
  15. Review
  16. Article
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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 4 institutions in 2 countries.

Lan LiuDepartment of Pathology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan Province, People's Republic of China.ORCID 0000-0002-0904-7417
Jing CaoDepartment of Pathology, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, People's Republic of China.
Jing ZhaoDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, People's Republic of China.
Xiangyu LiDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, People's Republic of China.
Zhenhe SuoDepartment of Pathology, The Norwegian Radium Hospital, Oslo University Hospital, Institute of Clinical Medicine, University of Oslo, Montebello, Oslo, Norway.
Huixiang LiDepartment of Pathology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan Province, People's Republic of China.
First Affiliated Hospital of Zhengzhou University · CNOslo University Hospital · NOThird Affiliated Hospital of Zhengzhou University · CNZhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOne of the remarkable metabolic characteristics of cancer cells is that they prefer glycolysis rather than oxidative phosphorylation (OXPHOS). Pyruvate dehydrogenase E1 alpha subunit (PDHA1) is an important prerequisite for OXPHOS. Our previous studies have shown that low level of PDHA1 protein expression in esophageal squamous cell cancer (ESCC) was correlated with poor prognosis. However, the effect of PDHA1 inhibition on metabolism and biological behavior of esophageal cancer cells remains unclear. METHODS AND

resultsIn this study, a KYSE450 PDHA1 knockout (KO) cell line of esophageal cancer was established by CRISPR/Cas9 technology. Then, the glycose metabolism, cell proliferation and migration abilities, chemotherapeutic tolerance and angiogenesis of the PDHA1 KO cells were investigated in vitro and in vivo. In the PDHA1 KO cells, the glycolysis and the consumption of glucose and glutamine were significantly enhanced, while the OXPHOS was significantly suppressed, implying Warburg effect in the PDHA1 KO cells. Furthermore, it was also proved in vitro experiments that the PDHA1 KO cell obtained proliferation advantage, as well as significantly greater chemotherapy tolerance and migration ability. Xenograft experiments discovered not only larger tumors but also increased angiogenesis in the PDHA1 KO cell group.

conclusionInhibition of

Indexed as

CRISPR/Cas9ESCCKYSE450PDHA1Warburg effectxenotransplantation

Identifiers

PMID31819487
PMCPMC6874154
OpenAlexW2985715129

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.