Evidence map›Paper›PMID 35039635›Full record

ArticleOncogene2022

MiR-378a inhibits glucose metabolism by suppressing GLUT1 in prostate cancer.

A Cannistraci, P Hascoet, A Ali, P Mundra, N W Clarke, V Pavet, R Marais

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. The Relationship between Circadian Rhythm and Cancer Disease.International journal of molecular sciences · 2024
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Depicting the Implication of miR-378a in Cancers.Technology in cancer research & treatment
    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 1 institution in 1 country.

A Cannistraci *Molecular Oncology Group, Cancer Research UK Manchester Institute, The University of Manchester, Alderley Park, Macclesfield, Cheshire, SK10 4TG, UK.
P Hascoet *Molecular Oncology Group, Cancer Research UK Manchester Institute, The University of Manchester, Alderley Park, Macclesfield, Cheshire, SK10 4TG, UK.ORCID http://orcid.org/0000-0003-4052-9059
A AliGenito-Urinary Cancer Research Group and the FASTMAN Prostate Cancer Centre for Excellence, Division of Cancer Sciences, Manchester Cancer Research Centre, The University of Manchester, 555 Wilmslow Road, Manchester, M20 4GJ, UK.ORCID http://orcid.org/0000-0002-8344-3776
P MundraMolecular Oncology Group, Cancer Research UK Manchester Institute, The University of Manchester, Alderley Park, Macclesfield, Cheshire, SK10 4TG, UK.
N W ClarkeGenito-Urinary Cancer Research Group and the FASTMAN Prostate Cancer Centre for Excellence, Division of Cancer Sciences, Manchester Cancer Research Centre, The University of Manchester, 555 Wilmslow Road, Manchester, M20 4GJ, UK.
V PavetMolecular Oncology Group, Cancer Research UK Manchester Institute, The University of Manchester, Alderley Park, Macclesfield, Cheshire, SK10 4TG, UK. valeria.pavet@cruk.manchester.ac.uk.ORCID http://orcid.org/0000-0002-4472-6503
R MaraisMolecular Oncology Group, Cancer Research UK Manchester Institute, The University of Manchester, Alderley Park, Macclesfield, Cheshire, SK10 4TG, UK. richard.marais@cruk.manchester.ac.uk.ORCID http://orcid.org/0000-0001-7484-4183
University of Manchester · GB

Funding

Cancer Research UK (CRUK) C5759/A20971Cancer Research UK (CRUK) C5759/A27412
6 · The paper itself

Abstract

Prostate cancer (PCa) is the fifth leading cause of cancer related deaths worldwide, in part due to a lack of molecular stratification tools that can distinguish primary tumours that will remain indolent from those that will metastasise. Amongst potential molecular biomarkers, microRNAs (miRs) have attracted particular interest because of their high stability in body fluids and fixed tissues. These small non-coding RNAs modulate several physiological and pathological processes, including cancer progression. Herein we explore the prognostic potential and the functional role of miRs in localised PCa and their relation to nodal metastasis. We define a 7-miR signature that is associated with poor survival independently of age, Gleason score, pathological T state, N stage and surgical margin status and that is also prognostic for disease-free survival in patients with intermediate-risk localised disease. Within our 7-miR signature, we show that miR-378a-3p (hereafter miR-378a) levels are low in primary tumours compared to benign prostate tissue, and also lower in Gleason score 8-9 compared to Gleason 6-7 PCa. We demonstrate that miR-378a impairs glucose metabolism and reduces proliferation in PCa cells through independent mechanisms, and we identify glucose transporter 1 (GLUT1) messenger RNA as a direct target of miR-378a. We show that GLUT1 inhibition hampers glycolysis, leading to cell death. Our data provides a rational for a new PCa stratification strategy based on miR expression, and it reveals that miR-378a and GLUT1 are potential therapeutic targets in highly aggressive glycolytic PCa.

Indexed as

MicroRNAsProstatic NeoplasmsCell Line, TumorCell ProliferationGlucoseGlucose Transporter Type 1HumansMaleGlucoseGlucose Transporter Type 1MicroRNAsSLC2A1 protein, human

Identifiers

PMID35039635
PMCPMC8897193
OpenAlexW4206274013

What OpenQuestion holds

Textmetadata
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.