Evidence map›Paper›PMID 26864945›Full record

ArticleJournal of cellular and molecular medicine2016

Anticancer efficacy of a nitric oxide-modified derivative of bifendate against multidrug-resistant cancer cells.

Zhiguang Ren, Xiaoke Gu, Bin Lu, Yaqiong Chen, Guojiang Chen, Jiannan Feng, Jizhen Lin, Yihua Zhang, Hui Peng

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  5. Review
  6. Antitumor Effects of L-citrulline on Hela Cervical Cancer Cell Lines.Anti-cancer agents in medicinal chemistry · 2022
    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

9 authors at 5 institutions in 2 countries.

Zhiguang RenDepartment of Environment and Pharmacy, Tianjin Institute of Health and Environmental Medicine, Beijing, China.
Xiaoke GuJiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Xuzhou Medical College, Xuzhou, China.
Bin LuSchool of Laboratory Medicine and Life Science, Wenzhou Medical College, Wenzhou, China.
Yaqiong ChenDepartment of Immunology, Institute of Basic Medical Sciences, Beijing, China.
Guojiang ChenDepartment of Immunology, Institute of Basic Medical Sciences, Beijing, China.
Jiannan FengDepartment of Immunology, Institute of Basic Medical Sciences, Beijing, China.
Jizhen LinDepartment of Otolaryngology, University of Minnesota Medical School, Minneapolis, MN, USA.
Yihua ZhangState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, China.
Hui PengDepartment of Environment and Pharmacy, Tianjin Institute of Health and Environmental Medicine, Beijing, China.
China Pharmaceutical University · CNCapital Medical University · CNInstitute of Basic Medical Sciences of the Chinese Academy of Medical SciencesUniversity of Minnesota Medical Center · USWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of multidrug resistance (MDR) not only actively transports a wide range of cytotoxic drugs across drug transporters but is also a complex interaction between a number of important cellular signalling pathways. Nitric oxide donors appear to be a new class of anticancer therapeutics for satisfying all the above conditions. Previously, we reported furoxan-based nitric oxide-releasing compounds that exhibited selective antitumour activity in vitro and in vivo. Herein, we demonstrate that bifendate (DDB)-nitric oxide, a synthetic furoxan-based nitric oxide-releasing derivative of bifendate, effectively inhibits the both sensitive and MDR tumour cell viability at a comparatively low concentration. Interestingly, the potency of DDB-nitric oxide is the independent of inhibition of the functions and expressions of three major ABC transporters. The mechanism of DDB-nitric oxide appears to be in two modes of actions by inducing mitochondrial tyrosine nitration and apoptosis, as well as by down-regulating HIF-1α expression and protein kinase B (AKT), extracellular signal-regulated kinases (ERK), nuclear factor κB (NF-κB) activation in MDR cells. Moreover, the addition of a typical nitric oxide scavenger significantly attenuated all the effects of DDB-nitric oxide, indicating that the cytotoxicity of DDB-nitric oxide is as a result of higher levels of nitric oxide release in MDR cancer cells. Given that acquired MDR to nitric oxide donors is reportedly difficult to achieve and genetically unstable, compound like DDB-nitric oxide may be a new type of therapeutic agent for the treatment of MDR tumours.

Indexed as

Antineoplastic AgentsApoptosisATP-Binding Cassette TransportersBiphenyl CompoundsDrug Resistance, MultipleDrug Resistance, NeoplasmExtracellular Signal-Regulated MAP KinasesHEK293 CellsHumansHypoxia-Inducible Factor 1, alpha SubunitK562 CellsMitochondriaNF-kappa BNitric OxideProto-Oncogene Proteins c-aktRNA, Messenger3-nitrotyrosineAntineoplastic AgentsATP-Binding Cassette TransportersbifendateBiphenyl CompoundsExtracellular Signal-Regulated MAP KinasesHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitNF-kappa BNitric OxideProto-Oncogene Proteins c-aktRNA, MessengerTyrosineanticancerbifendatemultidrug resistancenitric oxide

Identifiers

PMID26864945
PMCPMC4882976
OpenAlexW2281322224

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.