Evidence map›Paper›PMID 29331665›Full record

ArticleRedox biology2018

Blocking LPA-dependent signaling increases ovarian cancer cell death in response to chemotherapy.

LeAnn C Rogers, Ryan R Davis, Naveen Said, Thomas Hollis, Larry W Daniel

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Insights into the Role of Oxidative Stress in Ovarian Cancer.Oxidative medicine and cellular longevity · 2021
    Review
  14. Review
  15. Article
  16. 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

5 authors at 1 institution in 1 country.

LeAnn C RogersDept. of Biochemistry, Center for Structural Biology, Wake Forest School of Medicine, Winston-Salem, NC 27157, United States.
Ryan R DavisDept. of Biochemistry, Center for Structural Biology, Wake Forest School of Medicine, Winston-Salem, NC 27157, United States.
Naveen SaidDept. of Cancer Biology, Wake Forest School of Medicine, Winston-Salem, NC 27157, United States.
Thomas HollisDept. of Biochemistry, Center for Structural Biology, Wake Forest School of Medicine, Winston-Salem, NC 27157, United States. Electronic address: thollis@wakehealth.edu.
Larry W DanielDept. of Biochemistry, Center for Structural Biology, Wake Forest School of Medicine, Winston-Salem, NC 27157, United States. Electronic address: ldaniel@wakehealth.edu.
Wake Forest University · US

Funding

Tumor Tissue CoreP30CA012197 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Ruben A. Mesa · 1985 to 2026
$55.4M
Role of redox state in ovarian cancer response to cisplatinR01CA142838 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI DANIEL, LARRY W · 2010 to 2014
$1.4M
NCI NIH HHS P30 CA012197NCI NIH HHS R01 CA142838
6 · The paper itself

Abstract

The paradoxical role of reactive oxygen species in cell death versus cell survival establishes a delicate balance between chemotherapy efficacy and management of detrimental side effects. Normal proliferative signaling requires that cells remain inside a redox range that allows reversible protein oxidation to occur. Shifting the redox environment toward highly reducing or oxidizing states leads to cellular stress and cell death. Reactive oxygen species produced in response to Taxol and cisplatin treatment are necessary for effective cancer cell killing but the same ROS leads to damaging side effects in normal tissues. Combining antioxidants with chemotherapeutics to alleviate the unwanted side effects produces variable and often undesirable effects on cancer treatment. Here, we describe a more targeted method to improve ovarian cancer cell killing without the need for antioxidants. In ovarian cancer cells, lysophosphatidic acid (LPA) is a prominent growth factor that contributes to tumor survival and proliferation. We find that blocking LPA-dependent signaling with a specific receptor antagonist consistently increases cell death in response to both Taxol and cisplatin. We propose that inhibiting the upregulated growth factor-dependent signaling in cancer cells will target chemo-insensitivity, potentially lowering the necessary dose of the drugs and preventing harmful side effects.

Indexed as

AntioxidantsApoptosisCell DeathCell Line, TumorCell ProliferationCisplatinFemaleHumansLysophospholipidsOvarian NeoplasmsPaclitaxelReactive Oxygen SpeciesAntioxidantsCisplatinlysophosphatidic acidLysophospholipidsPaclitaxelReactive Oxygen SpeciesChemotherapyCisplatinLysophosphatidic acid (LPA)Ovarian cancerReactive oxygen species (ROS)Taxol

Identifiers

PMID29331665
PMCPMC5767563
OpenAlexW2781728052

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.