Evidence mapPaperPMID 27792451Full record

ArticleCell cycle (Georgetown, Tex.)2016

lncRNA NBR2 modulates cancer cell sensitivity to phenformin through GLUT1.

Xiaowen Liu, Boyi Gan

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

58 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
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  4. The role of curcumin in modulating circular RNAs and long non-coding RNAs in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
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  11. Decoding the regulatory roles of non-coding RNAs in cellular metabolism and disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. A ferroptosis defense mechanism mediated by glycerol-3-phosphate dehydrogenase 2 in mitochondria.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Xiaowen Liua Department of Experimental Radiation Oncology , University of Texas MD Anderson Cancer Center , Houston , TS , USA.
Boyi Gana Department of Experimental Radiation Oncology , University of Texas MD Anderson Cancer Center , Houston , TS , USA.
The University of Texas MD Anderson Cancer Center · US

Funding

Protocol Review and Monitoring SystemP30CA016672 · UNIVERSITY OF TX MD ANDERSON CAN CTR · 1985 to 2025
$57.3M
NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA181196NCI NIH HHS R01 CA190370
6 · The paper itself

Abstract

Biguanides, including metformin (widely used in diabetes treatment) and phenformin, are AMP-activated protein kinase (AMPK) activators and potential drugs for cancer treatment. A more in-depth understanding of how cancer cells adapt to biguanide treatment may provide important therapeutic implications to achieve more effective and rational cancer therapies. NBR2 is a glucose starvation-induced long non-coding RNA (lncRNA) that interacts with AMPK and regulates AMPK activity upon glucose starvation. Here we show that phenformin treatment induces NBR2 expression, and NBR2 deficiency sensitizes cancer cells to phenformin-induced cell death. Surprisingly, unlike glucose starvation, phenformin does not induce NBR2 interaction with AMPK, and correspondingly, NBR2 deficiency does not affect phenformin-induced AMPK activation. We further reveal that NBR2 depletion attenuates phenformin-induced glucose transporter GLUT1 expression and glucose uptake. GLUT1 deficiency sensitizes cancer cells to phenformin-induced cell death, whereas GLUT1 restoration in NBR2 deficient cells rescues the increased cell death upon phenformin treatment. Together, the results of our study reveal that NBR2-GLUT1 axis may serve as an adaptive response in cancer cells to survive in response to phenformin treatment, and identify a novel mechanism coupling lncRNA to biguanide-mediated biology.

Indexed as

AMP-Activated Protein KinasesCell DeathCell Line, TumorEnzyme ActivationGene Expression Regulation, NeoplasticGlucoseGlucose Transporter Type 1HEK293 CellsHumansMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesNeoplasmsPhenforminRNA, Long NoncodingSubcellular FractionsTOR Serine-Threonine KinasesAMP-Activated Protein KinasesGlucoseGlucose Transporter Type 1Mechanistic Target of Rapamycin Complex 1Multiprotein ComplexesNBR2 lncRNA, humanPhenforminRNA, Long NoncodingSLC2A1 protein, humanTOR Serine-Threonine KinasesTranscription FactorsAMPKbiguanideGLUT1long non-coding RNANBR2phenformin

Identifiers

PMID27792451
PMCPMC5224451
OpenAlexW2545504088

What Socratic 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 Socratic graph.