Evidence map›Paper›PMID 27614430›Full record

ArticleJournal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry2016

Bis(acetylacetonato)-oxidovanadium(IV) and sodium metavanadate inhibit cell proliferation via ROS-induced sustained MAPK/ERK activation but with elevated AKT activity in human pancreatic cancer AsPC-1 cells.

Jing-Xuan Wu, Yi-Hua Hong, Xiao-Gai Yang

Abstract read
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In one paragraph

Article in Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
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  10. Article
  11. Anticancer effect of sodium metavanadate on murine breast cancer both in vitro and in vivo.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2021
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Multi-modal Potentiation of Oncolytic Virotherapy by Vanadium Compounds.Molecular therapy : the journal of the American Society of Gene Therapy · 2018
    Article
  19. Vanadium Compounds as PTP Inhibitors.Molecules (Basel, Switzerland) · 2017
    Review
  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

3 authors at 1 institution in 1 country.

Jing-Xuan WuDepartment of Chemical Biology, School of Pharmaceutical Sciences, Peking University, Beijing, 100191, People's Republic of China.
Yi-Hua HongDepartment of Chemical Biology, School of Pharmaceutical Sciences, Peking University, Beijing, 100191, People's Republic of China.
Xiao-Gai YangDepartment of Chemical Biology, School of Pharmaceutical Sciences, Peking University, Beijing, 100191, People's Republic of China. yxg@bjmu.edu.cn.
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, the antiproliferative effect of bis(acetylacetonato)-oxidovanadium(IV) and sodium metavanadate and the underlying mechanisms were investigated in human pancreatic cancer cell line AsPC-1. The results showed that both exhibited an antiproliferative effect through inducing G2/M cell cycle arrest and can also cause elevation of reactive oxygen species (ROS) levels in cells. Moreover, the two vanadium compounds induced the activation of both PI3K/AKT and MAPK/ERK signaling pathways dose- and time-dependently, which could be counteracted with the antioxidant N-acetylcysteine. In the presence of MEK-1 inhibitor, the degradation of Cdc25C, inactivation of Cdc2 and accumulation of p21 were relieved. However, the treatment of AKT inhibitor did not cause any significant effect. Therefore, it demonstrated that the ROS-induced sustained MAPK/ERK activation rather than AKT contributed to vanadium compounds-induced G2/M cell cycle arrest. The current results also exhibited that the two vanadium compounds did not induce a sustained increase of ROS generation, but the level of ROS reached a plateau instead. The results revealed that an intracellular feedback loop may be against the elevated ROS level induced by vanadate or VO(acac)

Indexed as

AcetylcysteineBlotting, WesternCell Line, TumorCell ProliferationCell SurvivalDose-Response Relationship, DrugFree Radical ScavengersG2 Phase Cell Cycle CheckpointsGlutathioneHumansMAP Kinase Signaling SystemPancreatic NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesTime FactorsAcetylcysteineFree Radical ScavengersGlutathionePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesVanadatesAsPC-1 cellsExtracellular signal-regulated protein kinasePI3K/AKT signaling pathwayReactive oxygen speciesVanadium compounds

Identifiers

PMID27614430
OpenAlexW2515349108

What OpenQuestion holds

Textmetadata
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.