Evidence map›Paper›PMID 28753677›Full record

ArticlePloS one2017

Pyruvate kinase M2 is a poor prognostic marker of and a therapeutic target in ovarian cancer.

Tai-Kuang Chao, Tien-Shuo Huang, Yu-Ping Liao, Rui-Lan Huang, Po-Hsuan Su, Hueng-Yuan Shen, Hung-Cheng Lai, Yu-Chi Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 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
2.1field-weighted citation impact, top 13% 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, 54 citations in OpenAlex.

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  12. Ferroptosis, Metabolic Rewiring, and Endometrial Cancer.International journal of molecular sciences · 2023
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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 1 country.

Tai-Kuang ChaoGraduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan.
Tien-Shuo HuangLaboratory of Epigenetics and Cancer Stem Cells, National Defense Medical Centre, Taipei, Taiwan.
Yu-Ping LiaoLaboratory of Epigenetics and Cancer Stem Cells, National Defense Medical Centre, Taipei, Taiwan.
Rui-Lan HuangLaboratory of Epigenetics and Cancer Stem Cells, National Defense Medical Centre, Taipei, Taiwan.
Po-Hsuan SuLaboratory of Epigenetics and Cancer Stem Cells, National Defense Medical Centre, Taipei, Taiwan.
Hueng-Yuan ShenDepartment of Nuclear Medicine and PET center, Tri-Service General Hospital, National Defense Medical Centre, Taipei, Taiwan.
Hung-Cheng LaiGraduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan.
Yu-Chi WangGraduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan.
Taipei Medical University-Shuang Ho Hospital · TWNational Defense Medical Center · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pyruvate kinase M2 (PKM2) regulates glycolysis and oxidative phosphorylation; however, the role of PKM2 in ovarian cancer remains largely unknown. We investigated whether ovarian cancer metabolism could provide insight into the development of therapeutic strategies. We performed immunohistochemical staining for PKM2 on a tissue microarray for multivariate analysis. It revealed that patients exhibiting higher PKM2 expression were significantly associated with malignancy groups (p < 0.001) and pathogenesis models (p < 0.001), had poor progression-free survival rates (p = 0.01) as compared with patients exhibiting lower PKM2 levels, and yielded a hazard ratio of death of 2.02 (95% confidence interval: 0.70-5.85). In cell lines, PKM2 inhibitor significantly inhibited the glycolytic rate according to cellular glucose consumption (p < 0.001). We also utilized Seahorse assays to assess metabolism-related cell-specific factors and the impact of PKM2 inhibitors. Energy shifts as per Seahorse analysis showed attenuation of the extracellular acidification rate (p < 0.05) and no significant difference in oxygen-consumption rate in SKOV3 cells. Treatment with PKM2 inhibitor suppressed ovarian cancer growth and cell migration in vitro and inhibited tumor growth without significant toxicity in a xenograft study. PKM2 inhibition disturbed Warburg effects and inhibited ovarian cancer cell growth. Targeting PKM2 may constitute a promising therapy for patients with ovarian cancer, and clinical trials involving shikonin are warranted.

Indexed as

AnimalsBiomarkersCell Line, TumorCell SurvivalDisease-Free SurvivalEnzyme InhibitorsFemaleGlucoseHumansImmunohistochemistryLactic AcidMice, SCIDNaphthoquinonesOvarian NeoplasmsPositron-Emission TomographyPrognosisBiomarkersEnzyme InhibitorsGlucoseLactic AcidNaphthoquinonesPyruvate Kinaseshikonin

Identifiers

PMID28753677
PMCPMC5533430
OpenAlexW2741719757

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.