Evidence map›Paper›PMID 25779659›Full record

ArticleOncotarget2015

Phospho-TCTP as a therapeutic target of Dihydroartemisinin for aggressive breast cancer cells.

Maria Lucibello, Sara Adanti, Ester Antelmi, Dario Dezi, Stefania Ciafrè, Maria Luisa Carcangiu, Manuela Zonfrillo, Giuseppe Nicotera, Lorenzo Sica, Filippo De Braud and 1 more

Open access · diamondAbstract readComparative Study
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 60 citations in OpenAlex.

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  15. Review
  16. Dihydroartemisinin: A Potential Natural Anticancer Drug.International journal of biological sciences · 2021
    Review
  17. Article
  18. Review
  19. Article
  20. RSC advances · 2020
    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

11 authors at 4 institutions in 2 countries.

Maria LucibelloInstitute of Translational Pharmacology, National Research Council, Rome, Italy.
Sara AdantiInstitute of Translational Pharmacology, National Research Council, Rome, Italy.
Ester AntelmiMedical Oncology Department, Pathology and Molecular Biology Department, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy.
Dario DeziInstitute of Translational Pharmacology, National Research Council, Rome, Italy.
Stefania CiafrèInstitute of Translational Pharmacology, National Research Council, Rome, Italy.
Maria Luisa CarcangiuMedical Oncology Department, Pathology and Molecular Biology Department, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy.
Manuela ZonfrilloInstitute of Translational Pharmacology, National Research Council, Rome, Italy.
Giuseppe NicoteraInstitute of Translational Pharmacology, National Research Council, Rome, Italy.
Lorenzo SicaMedical Oncology Department, Pathology and Molecular Biology Department, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy.
Filippo De BraudMedical Oncology Department, Pathology and Molecular Biology Department, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy.
Pasquale PierimarchiInstitute of Translational Pharmacology, National Research Council, Rome, Italy.
Fondazione IRCCS Istituto Nazionale dei Tumori · ITIstituto di Farmacologia Traslazionale · ITNational Research Council · ITNational Academies of Sciences, Engineering, and Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Upregulation of Translationally Controlled Tumor Protein (TCTP) is associated with poorly differentiated aggressive tumors, including breast cancer, but the underlying mechanism(s) are still debated. Here, we show that in breast cancer cell lines TCTP is primarily localized in the nucleus, mostly in the phosphorylated form.The effects of Dihydroartemisinin (DHA), an anti-malaria agent that binds TCTP, were tested on breast cancer cells. DHA decreases cell proliferation and induces apoptotic cell death by targeting the phosphorylated form of TCTP. Remarkably, DHA enhances the anti-tumor effects of Doxorubicin in triple negative breast cancer cells resulting in an increased level of apoptosis. DHA also synergizes with Trastuzumab, used to treat HER2/neu positive breast cancers, to induce apoptosis of tumor cells.Finally, we present new clinical data that nuclear phospho-TCTP overexpression in primary breast cancer tissue is associated with high histological grade, increase expression of Ki-67 and with ER-negative breast cancer subtypes. Notably, phospho-TCTP expression levels increase in trastuzumab-resistant breast tumors, suggesting a possible role of phospho-TCTP as a new prognostic marker.In conclusion, the anti-tumor effect of DHA in vitro with conventional chemotherapeutics suggests a novel therapeutic strategy and identifies phospho-TCTP as a new promising target for advanced breast cancer.

Indexed as

AgedAntimalarialsAntineoplastic AgentsApoptosisArtemisininsBiomarkers, TumorBlotting, WesternBreastBreast NeoplasmsCell ProliferationCells, CulturedDrug SynergismDrug Therapy, CombinationFemaleHumansImmunoenzyme TechniquesAntimalarialsAntineoplastic AgentsArtemisininsartenimolBiomarkers, TumorRNA, MessengerTPT1 protein, humanTrastuzumabTumor Protein, Translationally-Controlled 1advanced breast cancercombination therapyDHAphospho-TCTPtarget therapy

Identifiers

PMID25779659
PMCPMC4467148
OpenAlexW1952266383

What OpenQuestion holds

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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.