Evidence map›Paper›PMID 28196146›Full record

ArticlePloS one2017

Chemotherapy induces adaptive drug resistance and metastatic potentials via phenotypic CXCR4-expressing cell state transition in ovarian cancer.

Hyun Hee Lee, Vanessa Bellat, Benedict Law

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.2field-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

32 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. Review
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  5. Article
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  7. Article
  8. Article
  9. Tumour invasion and dissemination.Biochemical Society transactions · 2022
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Cancer Stem Cells and Nucleolin as Drivers of Carcinogenesis.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
  15. Article
  16. Autophagy and Cancer Dormancy.Frontiers in oncology · 2021
    Review
  17. Review
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Hyun Hee LeeMolecular Imaging Innovations Institute, Department of Radiology, Weill Cornell Medicine, New York, New York, United States of America.
Vanessa BellatMolecular Imaging Innovations Institute, Department of Radiology, Weill Cornell Medicine, New York, New York, United States of America.
Benedict LawMolecular Imaging Innovations Institute, Department of Radiology, Weill Cornell Medicine, New York, New York, United States of America.ORCID http://orcid.org/0000-0001-7673-659X
Cornell University · US

Funding

Clinical and Translational Science CenterUL1TR000457 · NCATS · WEILL MEDICAL COLL OF CORNELL UNIV · PI IMPERATO-MCGINLEY, JULIANNE L · 2012 to 2016
$46.0M
NCATS NIH HHS UL1 TR000457
6 · The paper itself

Abstract

Ovarian cancer (OVC) patients who receive chemotherapy often acquire drug resistance within one year. This can lead to tumor reoccurrence and metastasis, the major causes of mortality. We report a transient increase of a small distinctive CXCR4High/CD24Low cancer stem cell population (CXCR4High) in A2780 and SKOV-3 OVC cell lines in response to cisplatin, doxorubicin, and paclitaxel, treatments. The withdrawal of the drug challenges reversed this cell-state transition. CXCR4High exhibits dormancy in drug resistance and mesenchymal-like invasion, migration, colonization, and tumor formation properties. The removal of this cell population from a doxorubicin-resistant A2780 lineage (A2780/ADR) recovered the sensitivity to drug treatments. A cytotoxic peptide (CXCR4-KLA) that can selectively target cell-surface CXCR4 receptor was further synthesized to investigate the therapeutic merits of targeting CXCR4High. This peptide was more potent than the conventional CXCR4 antagonists (AMD3100 and CTCE-9908) in eradicating the cancer stem cells. When used together with cytotoxic agents such as doxorubicin and cisplatin, the combined drug-peptide regimens exhibited a synergistic cell-killing effect on A2780, A2780/ADR, and SKOV-3. Our data suggested that chemotherapy could establish drug-resistant and tumor-initiating properties of OVC via reversible CXCR4 cell state transition. Therapeutic strategies designed to eradicate rather than antagonize CXCR4High might offer a far-reaching potential as supportive chemotherapy.

Indexed as

Cell Line, TumorCytotoxinsDoxorubicinDrug Resistance, NeoplasmFemaleHumansNeoplasm InvasivenessNeoplasm MetastasisNeoplasm ProteinsNeoplastic Stem CellsOvarian NeoplasmsPeptidesReceptors, CXCR4CXCR4 protein, humanCytotoxinsDoxorubicinNeoplasm ProteinsPeptidesReceptors, CXCR4

Identifiers

PMID28196146
PMCPMC5308810
OpenAlexW2589118911

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.