Evidence map›Paper›PMID 34533861›Full record

ArticleCancer science2021

Mannose and phosphomannose isomerase regulate energy metabolism under glucose starvation in leukemia.

Yusuke Saito, Mariko Kinoshita, Ai Yamada, Sayaka Kawano, Hong-Shan Liu, Sachiyo Kamimura, Midori Nakagawa, Syun Nagasawa, Tadao Taguchi, Shuhei Yamada and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

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  13. Comparative study ofScientific reports · 2024
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  15. Frontiers in pharmacology · 2024
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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

11 authors at 2 institutions in 1 country.

Yusuke SaitoDivision of Pediatrics, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.ORCID https://orcid.org/0000-0002-4605-5635
Mariko KinoshitaDivision of Pediatrics, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Ai YamadaDivision of Pediatrics, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Sayaka KawanoDivision of Pediatrics, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Hong-Shan LiuDivision of Pediatrics, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Sachiyo KamimuraDivision of Pediatrics, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Midori NakagawaDivision of Pediatrics, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Syun NagasawaDivision of Pediatrics, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Tadao TaguchiCenter for the Development of Pharmacy Education, Faculty of Pharmacy, Meijo University, Nagoya, Japan.
Shuhei YamadaDepartment of Pathobiochemistry, Faculty of Pharmacy, Meijo University, Nagoya, Japan.
Hiroshi MoritakeDivision of Pediatrics, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.ORCID https://orcid.org/0000-0001-5471-7646
University of Miyazaki · JPMeijo University · JP

Funding

Japanese Society of Hematology ResearchJSPS KAKENHI JP 18K16094JSPS KAKENHI JP19K17367JSPS KAKENHI JP 20K08735Shinnihon Foundation of Advanced Medical Treatment Research
6 · The paper itself

Abstract

Diverse metabolic changes are induced by various driver oncogenes during the onset and progression of leukemia. By upregulating glycolysis, cancer cells acquire a proliferative advantage over normal hematopoietic cells; in addition, these changes in energy metabolism contribute to anticancer drug resistance. Because leukemia cells proliferate by consuming glucose as an energy source, an alternative nutrient source is essential when glucose levels in bone marrow are insufficient. We profiled sugar metabolism in leukemia cells and found that mannose is an energy source for glycolysis, the tricarboxylic acid (TCA) cycle, and the pentose phosphate pathway. Leukemia cells express high levels of phosphomannose isomerase (PMI), which mobilizes mannose to glycolysis; consequently, even mannose in the blood can be used as an energy source for glycolysis. Conversely, suppression of PMI expression or a mannose load exceeding the processing capacity of PMI inhibited transcription of genes related to mitochondrial metabolism and the TCA cycle, therefore suppressing the growth of leukemia cells. High PMI expression was also a poor prognostic factor for acute myeloid leukemia. Our findings reveal a new mechanism for glucose starvation resistance in leukemia. Furthermore, the combination of PMI suppression and mannose loading has potential as a novel treatment for driver oncogene-independent leukemia.

Indexed as

Up-RegulationAnimalsCell Line, TumorCitric Acid CycleFemaleGene Expression Regulation, NeoplasticGlycolysisHumansK562 CellsLeukemiaMannoseMannose-6-Phosphate IsomeraseMicePentose Phosphate PathwayPrognosisTHP-1 CellsMannoseMannose-6-Phosphate Isomeraseactivation and metabolism of carcinogensglycolysishematopoietic organleukemia metabolismmannose metabolism

Identifiers

PMID34533861
PMCPMC8645730
OpenAlexW3201050288

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.