Evidence map›Paper›PMID 27074587›Full record

ArticleCell cycle (Georgetown, Tex.)2016

Autophagy protects ovarian cancer-associated fibroblasts against oxidative stress.

Qian Wang, Liang Xue, Xiaoyu Zhang, Shixia Bu, Xueliang Zhu, Dongmei Lai

Open access · hybridAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Glycolysis in the progression of pancreatic cancer.American journal of cancer research · 2022
    Review
  13. Article
  14. Article
  15. Autophagy and metabolism.The Kaohsiung journal of medical sciences · 2021
    Review
  16. Article
  17. Review
  18. Review
  19. The effects and the mechanisms of autophagy on the cancer-associated fibroblasts in cancer.Journal of experimental & clinical cancer research : CR · 2019
    Review
  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

6 authors at 4 institutions in 1 country.

Qian Wanga International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University , Shanghai , P. R. China.
Liang Xuec Shanghai Institute of Biochemistry and Cell Biology, SIBS, Chinese Academy of Sciences , Shanghai , China.
Xiaoyu Zhangc Shanghai Institute of Biochemistry and Cell Biology, SIBS, Chinese Academy of Sciences , Shanghai , China.
Shixia Bua International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University , Shanghai , P. R. China.
Xueliang Zhuc Shanghai Institute of Biochemistry and Cell Biology, SIBS, Chinese Academy of Sciences , Shanghai , China.
Dongmei Laia International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University , Shanghai , P. R. China.
Center for Excellence in Molecular Cell Science · CNShanghai Jiao Tong University · CNChinese Academy of Sciences · CNInternational Peace Maternity & Child Health Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RNA-Seq and gene set enrichment anylysis revealed that ovarian cancer associated fibroblasts (CAFs) are mitotically active compared with normal fibroblasts (NFs). Cellular senescence is observed in CAFs treated with H2O2 as shown by elevated SA-β-gal activity and p21 (WAF1/Cip1) protein levels. Reactive oxygen species (ROS) production and p21 (WAF1/Cip1) elevation may account for H2O2-induced CAFs cell cycle arrest in S phase. Blockage of autophagy can increase ROS production in CAFs, leading to cell cycle arrest in S phase, cell proliferation inhibition and enhanced sensitivity to H2O2-induced cell death. ROS scavenger NAC can reduce ROS production and thus restore cell viability. Lactate dehydrogenase A (LDHA), monocarboxylic acid transporter 4 (MCT4) and superoxide dismutase 2 (SOD2) were up-regulated in CAFs compared with NFs. There was relatively high lactate content in CAFs than in NFs. Blockage of autophagy decreased LDHA, MCT4 and SOD2 protein levels in CAFs that might enhance ROS production. Blockage of autophagy can sensitize CAFs to chemotherapeutic drug cisplatin, implicating that autophagy might possess clinical utility as an attractive target for ovarian cancer treatment in the future.

Indexed as

AcetylcysteineActinsAutophagyAutophagy-Related Protein 5Cancer-Associated FibroblastsCell ProliferationCells, CulturedCell SurvivalCyclin-Dependent Kinase Inhibitor p21FemaleFibroblastsHumansHydrogen PeroxideIsoenzymesLactate Dehydrogenase 5L-Lactate DehydrogenaseAcetylcysteineACTA2 protein, humanActinsAutophagy-Related Protein 5Cyclin-Dependent Kinase Inhibitor p21Hydrogen PeroxideIsoenzymesLactate Dehydrogenase 5L-Lactate DehydrogenaseMonocarboxylic Acid TransportersMuscle ProteinsReactive Oxygen SpeciesSLC16A4 protein, humanSuperoxide DismutaseSuperoxide Dismutase 2autophagyCAFsLDHAMCT4ovarian canceroxidative stressROSSOD2

Identifiers

PMID27074587
PMCPMC4889272
OpenAlexW2338007356

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.