Evidence map›Paper›PMID 28407774›Full record

ReviewMolecular cancer2017

ROS signaling under metabolic stress: cross-talk between AMPK and AKT pathway.

Yang Zhao, Xingbin Hu, Yajing Liu, Shumin Dong, Zhaowei Wen, Wanming He, Shuyi Zhang, Qiong Huang, Min Shi

Open access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 404 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
404citing papers in PubMed, 3 pooled it
14.7field-weighted citation impact, top 1% 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

404 citing papers in PubMed, 3 syntheses or guidelines pooled it, 713 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

344 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Yang ZhaoDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Xingbin HuDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yajing LiuDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Shumin DongDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Zhaowei WenDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Wanming HeDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Shuyi ZhangDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Qiong HuangDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Min ShiDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China. nfyyshimin@163.com.
Nanfang Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells are frequently confronted with metabolic stress in tumor microenvironments due to their rapid growth and limited nutrient supply. Metabolic stress induces cell death through ROS-induced apoptosis. However, cancer cells can adapt to it by altering the metabolic pathways. AMPK and AKT are two primary effectors in response to metabolic stress: AMPK acts as an energy-sensing factor which rewires metabolism and maintains redox balance. AKT broadly promotes energy production in the nutrient abundance milieu, but the role of AKT under metabolic stress is in dispute. Recent studies show that AMPK and AKT display antagonistic roles under metabolic stress. Metabolic stress-induced ROS signaling lies in the hub between metabolic reprogramming and redox homeostasis. Here, we highlight the cross-talk between AMPK and AKT and their regulation on ROS production and elimination, which summarizes the mechanism of cancer cell adaptability under ROS stress and suggests potential options for cancer therapeutics.

Indexed as

Stress, PhysiologicalAMP-Activated Protein KinasesAnimalsDisease ProgressionEnergy MetabolismHomeostasisHumansNeoplasmsOxidation-ReductionPhosphorylationProtein BindingProto-Oncogene Proteins c-aktReactive Oxygen SpeciesSignal TransductionAMP-Activated Protein KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesAKTAMPKFOXOMetabolic stressmTORReactive oxygen species

Identifiers

PMID28407774
PMCPMC5390360
OpenAlexW2607120474

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.