Evidence map›Paper›PMID 23202129›Full record

ArticleNature genetics2013

MCT1-mediated transport of a toxic molecule is an effective strategy for targeting glycolytic tumors.

Kivanç Birsoy, Tim Wang, Richard Possemato, Omer H Yilmaz, Catherine E Koch, Walter W Chen, Amanda W Hutchins, Yetis Gultekin, Tim R Peterson, Jan E Carette and 3 more

Open access · greenAbstract read
In one paragraph

Article in Nature genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed, 1 pooled it
11.1field-weighted citation impact, top 1% 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

121 citing papers in PubMed, 1 synthesis or guideline pooled it, 233 citations in OpenAlex.

  1. Pooled it
  2. Glucose and Lactate, Starters or Intermediates of Cancer Metabolic Rewiring.Advances in experimental medicine and biology · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Current Advances on Nanomaterials Interfering with Lactate Metabolism for Tumor Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review

61 more citing papers are in PubMed but not listed here.

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

13 authors at 4 institutions in 2 countries.

Kivanç BirsoyWhitehead Institute for Biomedical Research, Cambridge, Massachusetts, USA.
Tim Wang
Richard Possemato
Omer H Yilmaz
Catherine E Koch
Walter W Chen
Amanda W Hutchins
Yetis Gultekin
Tim R Peterson
Jan E Carette
Thijn R Brummelkamp
Clary B Clish
David M Sabatini
Whitehead Institute for Biomedical Research · USMassachusetts Institute of Technology · USBroad Institute · USThe Netherlands Cancer Institute · NL

Funding

Regulation of the mTOR Pathway By NutrientsR01CA103866 · NCI · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI WEISSMAN, JONATHAN S. · 2004 to 2021
$7.0M
Regulation of the Intestinal Stem Cell Niche in AgingK99AG045144 · NIA · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI YILMAZ, OMER · 2013 to 2014
$275k
Howard Hughes Medical InstituteNCI NIH HHS CA103866NCI NIH HHS R01 CA103866NIA NIH HHS K99 AG045144
6 · The paper itself

Abstract

There is increasing evidence that oncogenic transformation modifies the metabolic program of cells. A common alteration is the upregulation of glycolysis, and efforts to target glycolytic enzymes for anticancer therapy are under way. Here, we performed a genome-wide haploid genetic screen to identify resistance mechanisms to 3-bromopyruvate (3-BrPA), a drug candidate that inhibits glycolysis in a poorly understood fashion. We identified the SLC16A1 gene product, MCT1, as the main determinant of 3-BrPA sensitivity. MCT1 is necessary and sufficient for 3-BrPA uptake by cancer cells. Additionally, SLC16A1 mRNA levels are the best predictor of 3-BrPA sensitivity and are most elevated in glycolytic cancer cells. Furthermore, forced MCT1 expression in 3-BrPA-resistant cancer cells sensitizes tumor xenografts to 3-BrPA treatment in vivo. Our results identify a potential biomarker for 3-BrPA sensitivity and provide proof of concept that the selectivity of cancer-expressed transporters can be exploited for delivering toxic molecules to tumors.

Indexed as

AnimalsBiological TransportCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticGlycolysisHumansMiceMice, NudeMonocarboxylate Transport Protein 1Monocarboxylic Acid TransportersPyruvatesSymportersbromopyruvateMonocarboxylate Transport Protein 1Monocarboxylic Acid TransportersPyruvatesSymporters

Identifiers

PMID23202129
PMCPMC3530647
OpenAlexW2081651784

What OpenQuestion holds

Textmetadata
LicenceTDM
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.