Evidence map›Paper›PMID 25738776›Full record

ArticlePloS one2015

Isoform switch of pyruvate kinase M1 indeed occurs but not to pyruvate kinase M2 in human tumorigenesis.

Cheng Zhan, Li Yan, Lin Wang, Jun Ma, Wei Jiang, Yongxing Zhang, Yu Shi, Qun Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Loss of PKM2 in Lgr5Scientific reports · 2019
    Article
  10. Review
  11. The Multifarious Functions of Pyruvate Kinase M2 in Oral Cancer Cells.International journal of molecular sciences · 2018
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Contemporary Perspectives on the Warburg Effect Inhibition in Cancer Therapy.Cancer control : journal of the Moffitt Cancer Center
    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

8 authors at 5 institutions in 1 country.

Cheng ZhanDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Li YanDepartment of Radiation Oncology, Eye & ENT Hospital, Fudan University, Shanghai, China.
Lin WangDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Jun MaDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Wei JiangDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Yongxing ZhangDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Yu ShiDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Qun WangDepartment of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
The First Affiliated Hospital, Sun Yat-sen University · CNFudan University · CNEye & ENT Hospital of Fudan University · CNSun Yat-sen University · CNZhongshan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Muscle type of pyruvate kinase (PKM) is one of the key mediators of the Warburg effect and tumor metabolism. Due to alternative splicing, there are at least 12 known isoforms of the PKM gene, of which PKM1 and PKM2 are two major isoforms with only a 23 amino acid sequenced difference but quite different characteristics and functions. It was previously thought the isoform switch from PKM1 to PKM2 resulted in high PKM2 expression in tumors, providing a great advantage to tumor cells. However, this traditional view was challenged by two recent studies; one study claimed that this isoform switch does not occur during the Warburg effect; the other study asserted that the isoform switch is tissue-specific. Here, we re-analyzed the RNA sequencing data of 25 types of human tumors from The Cancer Genome Atlas Data Portal, and confirmed that PKM2 was the major isoform in the tumors and was highly elevated in addition to the entire PKM gene. We further demonstrated that the expression level of PKM1 significantly declined even though there was substantially increased expression of the entire PKM gene. The proportion of PKM1 in total transcript variants also significantly declined in tumors but the proportion of PKM2 did not change accordingly. Therefore, we conclude that the isoform switch of PKM1 does indeed occur, but it switches to other isoforms rather than PKM2. Considering the change in the expression levels of PKM1, PKM2 and the entire PKM gene, we propose that the upregulation of PKM2 is primarily due to elevated transcriptional levels of the entire PKM gene, instead of the isoform switch.

Indexed as

CarcinogenesisDatabases, GeneticGene Expression Regulation, NeoplasticHumansIsoenzymesMusclesNeoplasmsPyruvate KinaseRNA IsoformsRNA, MessengerSequence Analysis, RNAIsoenzymesPyruvate KinaseRNA IsoformsRNA, Messenger

Identifiers

PMID25738776
PMCPMC4349452
OpenAlexW2001355764

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.