Evidence map›Paper›PMID 28947972›Full record

ArticleOncotarget2017

PGC1α induced by reactive oxygen species contributes to chemoresistance of ovarian cancer cells.

Boyun Kim, Je Won Jung, Jaeyoung Jung, Youngjin Han, Dong Hoon Suh, Hee Seung Kim, Danny N Dhanasekaran, Yong Sang Song

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

43 citing papers in PubMed, 64 citations in OpenAlex.

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  18. Mitochondrial Control in Inflammatory Gastrointestinal Diseases.International journal of molecular sciences · 2022
    Review
  19. Elesclomol: a copper ionophore targeting mitochondrial metabolism for cancer therapy.Journal of experimental & clinical cancer research : CR · 2022
    Review
  20. 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

8 authors at 3 institutions in 2 countries.

Boyun KimCancer Research Institute, College of Medicine, Seoul National University, Seoul 03080, Korea.
Je Won JungResearch Institute of Agriculture and Life Sciences, Seoul National University, Seoul 08826, Korea.
Jaeyoung JungCancer Research Institute, College of Medicine, Seoul National University, Seoul 03080, Korea.
Youngjin HanCancer Research Institute, College of Medicine, Seoul National University, Seoul 03080, Korea.
Dong Hoon SuhDepartment of Obstetrics and Gynecology, Seoul National University Bundang Hospital, Seongnam 13620, Korea.
Hee Seung KimDepartment of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 03080, Korea.
Danny N DhanasekaranStephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73012, United States of America.
Yong Sang SongCancer Research Institute, College of Medicine, Seoul National University, Seoul 03080, Korea.
Seoul National University · KRSeoul National University Bundang Hospital · KRUniversity of Oklahoma Health Sciences Center · US

Funding

G Proteins and Their Receptors in Tumor Cell MetastasisR01CA116984 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI DHANASEKARAN, DANNY N. · 2007 to 2011
$1.5M
Regulation of JNK-signaling molecules by the gep oncogenesR01CA123233 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI DHANASEKARAN, DANNY N. · 2008 to 2013
$1.3M
NCI NIH HHS R01 CA116984NCI NIH HHS R01 CA123233
6 · The paper itself

Abstract

Malignant cells are subjected to high levels of oxidative stress that arise from the increased production of reactive oxygen species (ROS) due to their altered metabolism. They activate antioxidant mechanisms to relieve the oxidative stress, and thereby acquire resistance to chemotherapeutic agents. In the present study, we found that PGC1α, a key molecule that both increases mitochondrial biogenesis and activates antioxidant enzymes, enhances chemoresistance in response to ROS generated by exposure of cells to ovarian sphere-forming culture conditions. Cells in the cultured spheres exhibited stem cell-like characteristics, and maintained higher ROS levels than their parent cells. Intriguingly, scavenging ROS diminished the aldehyde dehydrogenase (ALDH)-positive cell population, and inhibited proliferation of the spheres. ROS production triggered PGC1α expression, which in turn caused changes to mitochondrial biogenesis and activity within the spheres. The drug-resistant phenotype was observed in both spheres and PGC1α-overexpressing parent cells, and conversely, PGC1α knockdown sensitized the spheres to cisplatin treatment. Similarly, floating malignant cells derived from patient ascitic fluid included an ALDH-positive population and exhibited the tendency of a positive correlation between expressions of multidrug resistance protein 1 (MDR1) and PGC1α. The present study suggests that ROS-induced PGC1α mediates chemoresistance, and represents a novel therapeutic target to overcome chemoresistance in ovarian cancer.

Indexed as

chemoresistancemitochondriaovarian cancerPGC1αROS

Identifiers

PMID28947972
PMCPMC5601140
OpenAlexW2736018139

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.