Evidence map›Paper›PMID 29207185›Full record

ArticleMolecular medicine reports2018

Novel multi‑kinase inhibitor, T03 inhibits Taxol‑resistant breast cancer.

Yan Li, Chunxia Liu, Ke Tang, Yan Chen, Kang Tian, Zhiqiang Feng, Jindong Chen

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 48% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

7 authors at 2 institutions in 2 countries.

Yan LiDepartment of Pharmacology, State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, P.R. China.
Chunxia LiuDepartment of Pharmacology, State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, P.R. China.
Ke TangDepartment of Pharmacology, State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, P.R. China.
Yan ChenDepartment of Pharmacology, State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, P.R. China.
Kang TianDepartment of Synthetic Medicinal Chemistry, Beijing Key Laboratory of Active Substance Discovery and Drugability Evaluation, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, P.R. China.
Zhiqiang FengDepartment of Synthetic Medicinal Chemistry, Beijing Key Laboratory of Active Substance Discovery and Drugability Evaluation, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, P.R. China.
Jindong ChenDepartment of Urology, University of Rochester Medical Center, Rochester, NY 14642, USA.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNUniversity of Rochester Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of kinase-associated signaling pathways is one of the leading causes of various malignant phenotypes in breast tumors. Strategies of drug discovery and development have investigated approaches to target the inhibition of protein kinase signaling. In the current study, the anti‑tumor activities of a novel multi‑kinase inhibitor, T03 were evaluated in breast cancer. T03 inhibited Taxol‑resistant breast cancer cell proliferation and induced cell cycle arrest and apoptosis in vitro and in vivo. The current results demonstrated that T03 downregulated c‑Raf, platelet‑derived growth factor receptor‑β and other kinases, thus inhibited Raf/mitogen‑activated protein kinase kinase/extracellular signal‑regulated kinase and Akt/mechanistic target of rapamycin survival pathways in MCF‑7 and MCF‑7/Taxol xenograft tumors. At a dose of 100 mg/kg, T03 inhibited tumor growth by 62.90 and 59.98% in tumor weight in MX‑1 and MX‑1/T xenograft models, respectively and by 62.60 and 60.22% in MCF‑7 and MCF‑7/T tumors, respectively. These data indicate that the novel multi‑kinase inhibitor, T03, may present as a potential compound to develop novel treatments against breast cancer and Taxol‑resistant breast tumors.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBreast NeoplasmsCell Cycle CheckpointsCell Line, TumorCell ProliferationDisease Models, AnimalDrug Resistance, NeoplasmFemaleHumansMicePaclitaxelProtein Kinase InhibitorsProto-Oncogene Proteins c-aktraf KinasesAntineoplastic AgentsPaclitaxelProtein Kinase InhibitorsProto-Oncogene Proteins c-aktraf Kinases

Identifiers

PMID29207185
PMCPMC5783483
OpenAlexW2769036944

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.