Evidence map›Paper›PMID 27806319›Full record

ArticleOncotarget2016

Ammonium tetrathiomolybdate treatment targets the copper transporter ATP7A and enhances sensitivity of breast cancer to cisplatin.

Cristine L Chisholm, Haitao Wang, Ada Hang-Heng Wong, Guelaguetza Vazquez-Ortiz, Weiping Chen, Xiaoling Xu, Chu-Xia Deng

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

40 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
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  7. Article
  8. Involvement of copper in cell death and cancer.Apoptosis : an international journal on programmed cell death · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. The Immune Response of Cancer Cells in Breast and Gynecologic Neoplasms.International journal of molecular sciences · 2024
    Review
  14. Article
  15. Review
  16. Review
  17. Review
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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 3 institutions in 2 countries.

Cristine L ChisholmGenetics of Development and Disease Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland MD, USA.
Haitao WangFaculty of Health Sciences, University of Macau, Macau SAR, China.
Ada Hang-Heng WongFaculty of Health Sciences, University of Macau, Macau SAR, China.
Guelaguetza Vazquez-OrtizGenetics of Development and Disease Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland MD, USA.
Weiping ChenGenomics Core Facility, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland MD, USA.
Xiaoling XuFaculty of Health Sciences, University of Macau, Macau SAR, China.
Chu-Xia DengFaculty of Health Sciences, University of Macau, Macau SAR, China.
National Institute of Diabetes and Digestive and Kidney Diseases · USUniversity of Macau · MONational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin is an effective breast cancer drug but resistance often develops over prolonged chemotherapy. Therefore, we performed a candidate approach RNAi screen in combination with cisplatin treatment to identify molecular pathways conferring survival advantages. The screen identified ATP7A as a therapeutic target. ATP7A is a copper ATPase transporter responsible for intercellular movement and sequestering of cisplatin. Pharmaceutical replacement for ATP7A by ammonium tetrathiomolybdate (TM) enhanced cisplatin treatment in breast cancer cells. Allograft and xenograft models in athymic nude mice treated with cisplatin/TM exhibited retarded tumor growth, reduced accumulation of cancer stem cells and decreased cell proliferation as compared to mono-treatment with cisplatin or TM. Cisplatin/TM treatment of cisplatin-resistant tumors reduced ATP7A protein levels, attenuated cisplatin sequestering by ATP7A, increased nuclear availability of cisplatin, and subsequently enhanced DNA damage and apoptosis. Microarray analysis of gene ontology pathways that responded uniquely to cisplatin/TM double treatment depicted changes in cell cycle regulation, specifically in the G1/S transition. These findings offer the potential to combat platinum-resistant tumors and sensitize patients to conventional breast cancer treatment by identifying and targeting the resistant tumors' unique molecular adaptations.

Indexed as

Angiogenesis InhibitorsAnimalsAntineoplastic Combined Chemotherapy ProtocolsBreast NeoplasmsCell Line, TumorCell ProliferationCisplatinCopper-Transporting ATPasesDrug SynergismGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMCF-7 CellsMice, NudeMolybdenumNeoplastic Stem CellsAngiogenesis InhibitorsCisplatinCopper-Transporting ATPasesMolybdenumtetrathiomolybdateATP7Abreast cancercisplatincopperresistancesequestering

Identifiers

PMID27806319
PMCPMC5341295
OpenAlexW2545208120

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.