Evidence map›Paper›PMID 29735611›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2018

Survivin Inhibitors Mitigate Chemotherapeutic Resistance in Breast Cancer Cells by Suppressing Genotoxic Nuclear Factor-

Wei Wang, Bo Zhang, Arul M Mani, Zhongzhi Wu, Yu Fan, Wei Li, Zhao-Hui Wu

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

17 citing papers in PubMed, 47 citations in OpenAlex.

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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

7 authors at 4 institutions in 2 countries.

Wei WangDepartments of Pathology and Laboratory Medicine (W.W., B.Z., Z.-H.W.), Physiology (A.M.M.), and Pharmaceutical Sciences (Z.W., W.L.), Center for Cancer Research (W.W., B.Z., Z.-H.W.), University of Tennessee Health Science Center, Memphis, Tennessee; and Cancer Institute, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China (Y.F.).
Bo ZhangDepartments of Pathology and Laboratory Medicine (W.W., B.Z., Z.-H.W.), Physiology (A.M.M.), and Pharmaceutical Sciences (Z.W., W.L.), Center for Cancer Research (W.W., B.Z., Z.-H.W.), University of Tennessee Health Science Center, Memphis, Tennessee; and Cancer Institute, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China (Y.F.).
Arul M ManiDepartments of Pathology and Laboratory Medicine (W.W., B.Z., Z.-H.W.), Physiology (A.M.M.), and Pharmaceutical Sciences (Z.W., W.L.), Center for Cancer Research (W.W., B.Z., Z.-H.W.), University of Tennessee Health Science Center, Memphis, Tennessee; and Cancer Institute, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China (Y.F.).
Zhongzhi WuDepartments of Pathology and Laboratory Medicine (W.W., B.Z., Z.-H.W.), Physiology (A.M.M.), and Pharmaceutical Sciences (Z.W., W.L.), Center for Cancer Research (W.W., B.Z., Z.-H.W.), University of Tennessee Health Science Center, Memphis, Tennessee; and Cancer Institute, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China (Y.F.).
Yu FanDepartments of Pathology and Laboratory Medicine (W.W., B.Z., Z.-H.W.), Physiology (A.M.M.), and Pharmaceutical Sciences (Z.W., W.L.), Center for Cancer Research (W.W., B.Z., Z.-H.W.), University of Tennessee Health Science Center, Memphis, Tennessee; and Cancer Institute, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China (Y.F.).
Wei LiDepartments of Pathology and Laboratory Medicine (W.W., B.Z., Z.-H.W.), Physiology (A.M.M.), and Pharmaceutical Sciences (Z.W., W.L.), Center for Cancer Research (W.W., B.Z., Z.-H.W.), University of Tennessee Health Science Center, Memphis, Tennessee; and Cancer Institute, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China (Y.F.) zwu6@uthsc.edu wli@uthsc.edu.
Zhao-Hui WuDepartments of Pathology and Laboratory Medicine (W.W., B.Z., Z.-H.W.), Physiology (A.M.M.), and Pharmaceutical Sciences (Z.W., W.L.), Center for Cancer Research (W.W., B.Z., Z.-H.W.), University of Tennessee Health Science Center, Memphis, Tennessee; and Cancer Institute, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China (Y.F.) zwu6@uthsc.edu wli@uthsc.edu.
Jiangsu University · CNUniversity of Tennessee Health Science Center · USAffiliated Hospital of Jiangsu University · CNWest Cancer Center · US

Funding

Selective Targeting Survivin for Cancer TherapyR01CA193609 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI LI, WEI · 2016 to 2020
$1.9M
Genotoxic NF-kB Signaling in CancerR01CA149251 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI WU, ZHAOHUI · 2011 to 2015
$1.5M
NCI NIH HHS R01 CA149251NCI NIH HHS R01 CA193609
6 · The paper itself

Abstract

Therapeutic resistance developed after chemotherapy and aggressive metastasis are the major causes of cancer-related death in patients with triple-negative breast cancer (TNBC). Survivin is the smallest member of the inhibitor-of-apoptosis proteins (IAPs) family, which plays critical roles in cell division and cell survival. High expression levels of survivin have been associated with therapeutic resistance in various cancers. We recently developed a novel small-molecule survivin inhibitor mimicking the IAP-binding motif of second mitochondria-derived activator of caspase, which showed high potency in promoting survivin degradation. Here, we show that survivin inhibitor MX106/MX107 suppresses TNBC cell proliferation. Moreover, MX106/MX107 synergized with chemotherapeutic drugs or radiation and significantly enhanced tumoricidal efficacy of genotoxic treatments. Mechanistically, MX106/MX107 induced degradation of XIAP and/or cIAP1, which inhibited nuclear factor

Indexed as

ApoptosisBreast NeoplasmsCell CycleCell Line, TumorDose-Response Relationship, DrugDoxorubicinDrug Resistance, NeoplasmDrug SynergismHumansMutagensNF-kappa BQuinolinesSignal TransductionSurvivinX-Linked Inhibitor of Apoptosis ProteinDoxorubicinMutagensNF-kappa BQuinolinesSurvivinX-Linked Inhibitor of Apoptosis Protein

Identifiers

PMID29735611
PMCPMC6038029
OpenAlexW2802441329

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.