ReviewCell cycle (Georgetown, Tex.)2009
Growth controls connect: interactions between c-myc and the tuberous sclerosis complex-mTOR pathway.
Review in Cell cycle (Georgetown, Tex.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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.
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.
Who cites it
30 citing papers in PubMed, 56 citations in OpenAlex.
- Machine Learning-Based Predictive Modeling Maximizes the Efficacy of mTOR/p53 Co-Targeting Therapy Against AML.Cancer science · 2025Article
- Article
- Regulation and clinical potential of telomerase reverse transcriptase (TERT/hTERT) in breast cancer.Cell communication and signaling : CCS · 2023Review
- Obesity under the moonlight of c-MYC.Frontiers in cell and developmental biology · 2023Review
- Ribosomal Protein S6: A Potential Therapeutic Target against Cancer?International journal of molecular sciences · 2021Review
- Review
- An IRF4-MYC-mTORC1 Integrated Pathway Controls Cell Growth and the Proliferative Capacity of Activated B Cells during B Cell Differentiation In Vivo.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Upregulation of the pathogenic transcription factor SPI1/PU.1 in tuberous sclerosis complex and focal cortical dysplasia by oxidative stress.Brain pathology (Zurich, Switzerland) · 2021Article
- Poly-L-arginine promotes asthma angiogenesis through induction of FGFBP1 in airway epithelial cells via activation of the mTORC1-STAT3 pathway.Cell death & disease · 2021Article
- RABL6A Promotes Pancreatic Neuroendocrine Tumor Angiogenesis and Progression In Vivo.Biomedicines · 2021Article
- Beyond Protein Synthesis; The Multifaceted Roles of Tuberin in Cell Cycle Regulation.Frontiers in cell and developmental biology · 2021Review
- MYC-binding lncRNA EPIC1 promotes AKT-mTORC1 signaling and rapamycin resistance in breast and ovarian cancer.Molecular carcinogenesis · 2020Article
- Let-7 derived from endometrial extracellular vesicles is an important inducer of embryonic diapause in mice.Science advances · 2020Article
- Rapamycin and dexamethasone during pregnancy prevent tuberous sclerosis complex-associated cystic kidney disease.JCI insight · 2020Article
- Loss of FOXP3 and TSC1 Accelerates Prostate Cancer Progression through Synergistic Transcriptional and Posttranslational Regulation of c-MYC.Cancer research · 2019Article
- A functional mammalian target of rapamycin complex 1 signaling is indispensable for c-Myc-driven hepatocarcinogenesis.Hepatology (Baltimore, Md.) · 2017Article
- Article
- Therapeutic dosages of aspirin counteract the IL-6 induced pro-tumorigenic effects by slowing down the ribosome biogenesis rate.Oncotarget · 2016Article
- Inhibition of mTORC1 signaling sensitizes hepatocellular carcinoma cells to glycolytic stress.American journal of cancer research · 2016Article
- mTOR/MYC Axis Regulates O-GlcNAc Transferase Expression and O-GlcNAcylation in Breast Cancer.Molecular cancer research : MCR · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Among other signals, cell growth is particularly controlled by the target of rapamycin (TOR) pathway that includes the tuberous sclerosis complex genes (TSC1/2), and through transcriptional effects regulated by c-myc. Overexpression of Drosophila Myc and TSC1/2 cause opposing growth and proliferation defects. Despite this relationship, direct regulatory connections between Myc and the TSC have only recently been evaluated. Other than studies of p53 regulation, little consideration has been given to transcriptional regulation of the TSC genes. Here we review evidence that transcriptional controls are potentially important regulators of TSC2 expression, and that Myc is a direct repressor of its expression. Since tuberin loss de-represses Myc protein, the connection between these two growth regulators is positioned to act as a feed-forward loop that would amplify the oncogenic effects of decreased tuberin or increased Myc. Further experiments will be needed to clarify the mechanisms underlying this important connection, and evaluate its overall contribution to cancers caused by TSC loss or Myc gain.
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Registered trials
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.