Evidence map›Paper›PMID 26500118›Full record

ArticleDigestive diseases and sciences2016

PKM2 Promotes Cell Survival and Invasion Under Metabolic Stress by Enhancing Warburg Effect in Pancreatic Ductal Adenocarcinoma.

Chenggang Li, Zhiming Zhao, Zhipeng Zhou, Rong Liu

Abstract read
PubMed Publisher
In one paragraph

Article in Digestive diseases and sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 2 pooled it
1.3field-weighted citation impact, top 22% 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

40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 52 citations in OpenAlex.

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

4 authors at 1 institution in 1 country.

Chenggang LiDepartment of Surgical Oncology, Chinese PLA General Hospital, 28#, Fuxing Road, Beijing, 100853, People's Republic of China. drchengg@126.com.
Zhiming ZhaoDepartment of Surgical Oncology, Chinese PLA General Hospital, 28#, Fuxing Road, Beijing, 100853, People's Republic of China.
Zhipeng ZhouDepartment of Surgical Oncology, Chinese PLA General Hospital, 28#, Fuxing Road, Beijing, 100853, People's Republic of China.
Rong LiuDepartment of Surgical Oncology, Chinese PLA General Hospital, 28#, Fuxing Road, Beijing, 100853, People's Republic of China.
Chinese PLA General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPyruvate kinase isoenzyme M2 (PKM2) is an essential enzyme involved in the regulation of aerobic glycolysis in cancer cells and promotes the translation between glycolytic flux and biosynthesis of cellular building blocks.

aimOur present study aims to explore the expression pattern and underlying cellular functions of PKM2 in pancreatic ductal adenocarcinoma (PDAC) under metabolic stress.

methodsOncomine database and a tissue microarray (n = 90) were used to investigate the expression pattern of PKM2 and its clinicopathological findings. In vitro proliferation, apoptosis and invasion assays were used to determine the role and related mechanism of PKM2 in PDAC.

resultsData from Oncomine database and our tissue microarray show that PKM2 is significantly elevated in PDAC specimens compared with the corresponding normal tissues. Kaplan-Meier survival analysis shows that higher expression of PKM2 is closely correlated with a poor prognosis of patients with PDAC. Under metabolic stress, suppression of PKM2 expression in PANC-1 and AsPC-1 cells results in decreased cell survival, increased caspase-3/7 activity, and reduced invasive potential, and these effects can be reversed by reintroduction of PKM2. Furthermore, sh-PKM2 cells show a significant decreased Warburg effect compared with sh-Ctrl cells as demonstrated by reduced glucose consumption and lactate production. Treatment with 2-deoxy-D-glucose, a glycolysis inhibitor, completely blocks the influences of PKM2 on cell survival and invasion.

conclusionsOur study reveals that silencing of PKM2 exhibits a tumor-suppressive role through altered Warburg effect and suggests that targeting PKM2 might serve as a potential therapeutic target for PDAC.

Indexed as

Gene Expression Regulation, NeoplasticAgedApoptosisBlotting, WesternCarcinoma, Pancreatic DuctalCarrier ProteinsCaspase 3Caspase 7Cell Line, TumorCell SurvivalFemaleGlucoseHumansImmunohistochemistryKaplan-Meier EstimateMaleCarrier ProteinsCASP3 protein, humanCASP7 protein, humanCaspase 3Caspase 7GlucoseMembrane ProteinsThyroid Hormone-Binding ProteinsThyroid HormonesInvasionPancreatic ductal adenocarcinomaPKM2SurvivalWarburg effect

Identifiers

PMID26500118
OpenAlexW1885007540

What OpenQuestion holds

Textmetadata
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.