Evidence map›Paper›PMID 24275666›Full record

ArticleThe Journal of biological chemistry2014

Hyperactivation of mammalian target of rapamycin complex 1 (mTORC1) promotes breast cancer progression through enhancing glucose starvation-induced autophagy and Akt signaling.

Yongqiang Chen, Huijun Wei, Fei Liu, Jun-Lin Guan

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. 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
1.3field-weighted citation impact, top 21% 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, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Role of TSC1 in physiology and diseases.Molecular and cellular biochemistry · 2021
    Review
  6. Article
  7. Review
  8. The paradox of autophagy in Tuberous Sclerosis Complex.Genetics and molecular biology · 2021
    Article
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  10. Article
  11. Article
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  19. Review
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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

4 authors at 1 institution in 2 countries.

Yongqiang ChenFrom the Divisions of Molecular Medicine and Genetics, Department of Internal Medicine, and.
Huijun Wei
Fei Liu
Jun-Lin Guan
University of Michigan–Ann Arbor · US

Funding

The Mechanisms of Bone Mass Regulation by FIP200R01AR062030 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LIU, FEI · 2012 to 2016
$1.7M
Genetic Analysis of FAK kinase and scaffold functions in breast cancerR01CA163493 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GUAN, JUN-LIN · 2012 to 2016
$1.6M
Molecular Analysis of Signal Transduction in Cancer Development and ProgressionR01CA150926 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GUAN, JUN-LIN · 2010 to 2014
$1.4M
NCI NIH HHS CA150926NCI NIH HHS CA163493NCI NIH HHS R01 CA150926NCI NIH HHS R01 CA163493NIAMS NIH HHS R01 AR062030
6 · The paper itself

Abstract

The mammalian target of rapamycin complex 1 (mTORC1) is a master regulator of cell growth and proliferation. Recent studies have suggested that constitutive activation of mTORC1 in normal cells could lead to malignant tumor development in several tissues. However, the mechanisms of mTORC1 hyperactivation to promote the growth and metastasis of breast or other cancers are still not well characterized. Here, using a new inducible deletion system, we show that deletion of Tsc1 in mouse primary mammary tumor cells, either before or after their transplantation, significantly increased their growth in vivo. The increase in tumor growth was completely rescued by rapamycin treatment, suggesting a major contribution from mTORC1 hyperactivation. Interestingly, glucose starvation-induced autophagy, but not amino acid starvation-induced autophagy, was increased significantly in Tsc1-null tumor cells. Further analysis of these cells also showed an increased Akt activation but no significant changes in Erk signaling. Together, these results provide insights into the mechanism by which hyperactivation of mTORC1 promotes breast cancer progression through increasing autophagy and Akt activation in vivo.

Indexed as

AnimalsAutophagyCell SurvivalFemaleGlucoseHEK293 CellsHumansImmunoblottingMammary Neoplasms, ExperimentalMechanistic Target of Rapamycin Complex 1MiceMice, Inbred C57BLMice, KnockoutMice, NudeMice, TransgenicMultiprotein ComplexesGlucoseMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesTSC1 protein, humanTsc1 protein, mouseTuberous Sclerosis Complex 1 ProteinTumor Suppressor ProteinsAutophagyBreast CancerMousemTOR Complex (mTORC)Signaling

Identifiers

PMID24275666
PMCPMC3887183
OpenAlexW1965704830

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.