Evidence map›Paper›PMID 26330167›Full record

ArticleScientific reports2015

BA-j as a novel CDK1 inhibitor selectively induces apoptosis in cancer cells by regulating ROS.

Shixuan Zhang, Yongming Bao, Xiulan Ju, Kangjian Li, Haiyan Shang, Lisha Ha, Yuan Qian, Liang Zou, Xiaodan Sun, Jing Li and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Reactive oxygen species in haematopoiesis: leukaemic cells take a walk on the wild side.Journal of experimental & clinical cancer research : CR · 2018
    Review
  9. Article
  10. 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

12 authors at 2 institutions in 1 country.

Shixuan ZhangState Key Laboratory of Fine Chemicals, School of Pharmaceutical Science and Technology, Dalian University of Technology, Dalian, Liaoning, China.
Yongming BaoSchool of Bioscience and Technology, Dalian University of Technology, Dalian, Liaoning, China.
Xiulan JuCollege of Vocational and Technical, Dalian University, Dalian, Liaoning, China.
Kangjian LiState Key Laboratory of Fine Chemicals, School of Pharmaceutical Science and Technology, Dalian University of Technology, Dalian, Liaoning, China.
Haiyan ShangSchool of Bioscience and Technology, Dalian University of Technology, Dalian, Liaoning, China.
Lisha HaState Key Laboratory of Fine Chemicals, School of Pharmaceutical Science and Technology, Dalian University of Technology, Dalian, Liaoning, China.
Yuan QianState Key Laboratory of Fine Chemicals, School of Pharmaceutical Science and Technology, Dalian University of Technology, Dalian, Liaoning, China.
Liang ZouState Key Laboratory of Fine Chemicals, School of Pharmaceutical Science and Technology, Dalian University of Technology, Dalian, Liaoning, China.
Xiaodan SunState Key Laboratory of Fine Chemicals, School of Pharmaceutical Science and Technology, Dalian University of Technology, Dalian, Liaoning, China.
Jing LiState Key Laboratory of Fine Chemicals, School of Pharmaceutical Science and Technology, Dalian University of Technology, Dalian, Liaoning, China.
Qianru WangState Key Laboratory of Fine Chemicals, School of Pharmaceutical Science and Technology, Dalian University of Technology, Dalian, Liaoning, China.
Qingyu FanState Key Laboratory of Fine Chemicals, School of Pharmaceutical Science and Technology, Dalian University of Technology, Dalian, Liaoning, China.
Dalian University · CNDalian University of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclin-dependent kinase 1 (CDK1) is the only necessary CDK in cell proliferation and a novel target in the development of anticancer drugs. 8-Hydroxypiperidinemethyl-baicalein (BA-j) is a novel selective CDK1 inhibitor with broad spectrum anti-cancer activity (IC50 12.3 μM) and 2 tumor xenografts. Because of the differential mechanisms controlling redox-states in normal and cancer cells, BA-j can capture oxygen free radicals ((·)O2(-)) and selectively increase the level of H2O2 in cancer cells, thereby specifically oxidize and activate the intrinsic apoptosis pathway bypassing the extrinsic death receptor pathway, thus inducing apoptosis in cancer cells rather than in normal cells. BA-j is different from cytotoxic anticancer drugs which can activate both the intrinsic apoptosis pathway and the extrinsic death receptor pathway, and therefore harm normal cells while killing cancer cells. The molecular and biochemical mechanisms of reactive oxygen species (ROS) regulation suggest that BA-j may be developed into a novel anticancer agent.

Indexed as

AcetylcysteineAnimalsAntineoplastic AgentsApoptosisCDC2 Protein KinaseCell Line, TumorCell ProliferationDrug Evaluation, PreclinicalFas Ligand ProteinFlavonesHumansInhibitory Concentration 50MacacaMetabolic Networks and PathwaysPiperidinesProtein Kinase Inhibitors8-hydroxypiperidinylmethylbaicaleinAcetylcysteineAntineoplastic AgentsCDC2 Protein KinaseFas Ligand ProteinFlavonesPiperidinesProtein Kinase InhibitorsReactive Oxygen Species

Identifiers

PMID26330167
PMCPMC4557050
OpenAlexW1235120122

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.