Evidence map›Paper›PMID 24626155›Full record

ArticlePloS one2014

Oleanolic acid suppresses aerobic glycolysis in cancer cells by switching pyruvate kinase type M isoforms.

Jia Liu, Ning Wu, Leina Ma, Ming Liu, Ge Liu, Yuyan Zhang, Xiukun Lin

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. 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
2.9field-weighted citation impact, top 9% 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, 71 citations in OpenAlex.

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  12. Frontiers in molecular biosciences · 2023
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  13. Overview of Cancer Metabolism and Signaling Transduction.International journal of molecular sciences · 2022
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  18. Targeting Mitochondrial Metabolism in Prostate Cancer with Triterpenoids.International journal of molecular sciences · 2021
    Review
  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

7 authors at 3 institutions in 1 country.

Jia LiuInstitutes of Oceanology, Chinese Academy of Sciences, Qingdao, China; Graduate School, University of Chinese Academy of Sciences, Beijing, China.
Ning WuInstitutes of Oceanology, Chinese Academy of Sciences, Qingdao, China.
Leina MaDepartment of Molecular Biology, School of Medicine and Pharmacy, Ocean University of China, Qingdao, China.
Ming LiuInstitutes of Oceanology, Chinese Academy of Sciences, Qingdao, China.
Ge LiuInstitutes of Oceanology, Chinese Academy of Sciences, Qingdao, China; Graduate School, University of Chinese Academy of Sciences, Beijing, China.
Yuyan ZhangInstitutes of Oceanology, Chinese Academy of Sciences, Qingdao, China.
Xiukun LinInstitutes of Oceanology, Chinese Academy of Sciences, Qingdao, China; Department of Pharmacology, Capital Medical University, Beijing, China.
Institute of Oceanology · CNChinese Academy of Sciences · CNOcean University of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Warburg effect, one of the hallmarks for cancer cells, is characterized by metabolic switch from mitochondrial oxidative phosphorylation to aerobic glycolysis. In recent years, increased expression level of pyruvate kinase M2 (PKM2) has been found to be the culprit of enhanced aerobic glycolysis in cancer cells. However, there is no agent inhibiting aerobic glycolysis by targeting PKM2. In this study, we found that Oleanolic acid (OA) induced a switch from PKM2 to PKM1, and consistently, abrogated Warburg effect in cancer cells. Suppression of aerobic glycolysis by OA is mediated by PKM2/PKM1 switch. Furthermore, mTOR signaling was found to be inactivated in OA-treated cancer cells, and mTOR inhibition is required for the effect of OA on PKM2/PKM1 switch. Decreased expression of c-Myc-dependent hnRNPA1 and hnRNPA1 was responsible for OA-induced switch between PKM isoforms. Collectively, we identified that OA is an antitumor compound that suppresses aerobic glycolysis in cancer cells and there is potential that PKM2 may be developed as an important target in aerobic glycolysis pathway for developing novel anticancer agents.

Indexed as

Antineoplastic AgentsBreast NeoplasmsCarrier ProteinsCell Line, TumorFemaleGene Expression Regulation, NeoplasticGlycolysisHeterogeneous Nuclear Ribonucleoprotein A1Heterogeneous-Nuclear Ribonucleoprotein Group A-BHumansMaleMCF-7 CellsMembrane ProteinsMitochondriaOleanolic AcidOxidative PhosphorylationAntineoplastic AgentsCarrier ProteinsHeterogeneous Nuclear Ribonucleoprotein A1Heterogeneous-Nuclear Ribonucleoprotein Group A-BhnRNPA1 protein, humanMembrane ProteinsOleanolic AcidProtein IsoformsProto-Oncogene Proteins c-mycPyruvate KinaseThyroid Hormone-Binding ProteinsThyroid Hormones

Identifiers

PMID24626155
PMCPMC3953484
OpenAlexW2014750380

What OpenQuestion holds

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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.