Evidence map›Paper›PMID 31323788›Full record

ArticleCancers2019

Inhibition of DNA Repair Mechanisms and Induction of Apoptosis in Triple Negative Breast Cancer Cells Expressing the Human Herpesvirus 6 U94.

Francesca Caccuri, Michele Sommariva, Stefania Marsico, Francesca Giordano, Alberto Zani, Arianna Giacomini, Cornel Fraefel, Andrea Balsari, Arnaldo Caruso

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
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 4 institutions in 2 countries.

Francesca CaccuriDepartment of Molecular and Translational Medicine, University of Brescia, Brescia 25123, Italy.
Michele SommarivaDipartimento di Scienze Biomediche per la Salute, Università degli Studi di Milano, Milan 20133, Italy.
Stefania MarsicoDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Arcavacata di Rende, Cosenza 87036, Italy.ORCID 0000-0003-1598-0526
Francesca GiordanoDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Arcavacata di Rende, Cosenza 87036, Italy.
Alberto ZaniDepartment of Molecular and Translational Medicine, University of Brescia, Brescia 25123, Italy.
Arianna GiacominiDepartment of Molecular and Translational Medicine, University of Brescia, Brescia 25123, Italy.
Cornel FraefelInstitute of Virology, University of Zurich, Zurich 8057, Switzerland.
Andrea BalsariDipartimento di Scienze Biomediche per la Salute, Università degli Studi di Milano, Milan 20133, Italy.
Arnaldo CarusoDepartment of Molecular and Translational Medicine, University of Brescia, Brescia 25123, Italy. arnaldo.caruso@unibs.it.
University of Brescia · ITUniversity of Calabria · ITUniversity of Milan · ITUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) accounts for 15-20% of all breast cancers. In spite of initial good response to chemotherapy, the prognosis of TNBC remains poor and no effective specific targeted therapy is readily available. Recently, we demonstrated the ability of U94, the latency gene of human herpes virus 6 (HHV-6), to interfere with proliferation and with crucial steps of the metastatic cascade by using MDA-MB 231 TNBC breast cancer cell line. U94 expression was also associated with a partial mesenchymal-to-epithelial transition (MET) of cells, which displayed a less aggressive phenotype. In this study, we show the ability of U94 to exert its anticancer activity on three different TNBC cell lines by inhibiting DNA damage repair genes, cell cycle and eventually leading to cell death following activation of the intrinsic apoptotic pathway. Interestingly, we found that U94 acted synergistically with DNA-damaging drugs. Overall, we provide evidence that U94 is able to combat tumor cells with different mechanisms, thus attesting for the great potential of this molecule as a multi-target drug in cancer therapy.

Indexed as

apoptosiscell cycleDNA repairgene expression profileHHV-6 U94HSV-1 amplicon vectortriple negative breast cancer cells

Identifiers

PMID31323788
PMCPMC6679437
OpenAlexW2960636544

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.