ArticleCancer letters2015
Rapamycin-induced G1 cell cycle arrest employs both TGF-β and Rb pathways.
Article in Cancer letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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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.
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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.
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Who cites it
36 citing papers in PubMed, 65 citations in OpenAlex.
- Divergence between neural and retinal lineage specification during human brain development by signal transduction.Journal of advanced research · 2026Article
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- mTORC1 regulates the proliferation of SOX9Histochemistry and cell biology · 2025Article
- Prim-O-glucosylcimifugin alleviates influenza virus-induced pneumonia in mice by inhibiting the TGF-β1/PI3KCD/MSK2/RELA signalling pathway.Archives of virology · 2024Article
- Regulatory role of the mTOR signaling pathway in autophagy and mesangial proliferation in IgA nephropathy.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- Crosstalk between m6A modification and autophagy in cancer.Cell & bioscience · 2024Review
- Stigmasterol Exerts an Anti-Melanoma Property through Down-Regulation of Reactive Oxygen Species and Programmed Cell Death Ligand 1 in Melanoma Cells.Antioxidants (Basel, Switzerland) · 2024Article
- Molecular and therapeutic insights of rapamycin: a multi-faceted drug from Streptomyces hygroscopicus.Molecular biology reports · 2023Review
- Review
- New Visions on Natural Products and Cancer Therapy: Autophagy and Related Regulatory Pathways.Cancers · 2022Review
- Article
- Tumor microenvironment in non-melanoma skin cancer resistance to photodynamic therapy.Frontiers in oncology · 2022Review
- Theabrownins Produced via Chemical Oxidation of Tea Polyphenols Inhibit Human Lung Cancer CellsFrontiers in nutrition · 2022Article
- Cancer cells with defective RB and CDKN2A are resistant to the apoptotic effects of rapamycin.Cancer letters · 2021Article
- Metformin impairs cisplatin resistance effects in A549 lung cancer cells through mTOR signaling and other metabolic pathways.International journal of oncology · 2021Article
- Optimization of BCG Therapy Targeting Neutrophil Extracellular Traps, Autophagy, and miRNAs in Bladder Cancer: Implications for Personalized Medicine.Frontiers in medicine · 2021Review
- Repression of Smad4 by MicroRNA-1285 moderates TGF-β-induced epithelial-mesenchymal transition in proliferative vitreoretinopathy.PloS one · 2021Article
- Albumin promotes the progression of fibroblasts through late GCell cycle (Georgetown, Tex.) · 2020Article
- Cellular and molecular mechanisms of xenobiotics-induced premature senescence.Toxicology research · 2020Review
- Infrared-A Irradiation-induced Inhibition of Human Keratinocyte Proliferation and Potential Mechanisms.Photochemistry and photobiology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The mammalian target of rapamycin complex 1 (mTORC1) is a critical regulator of G1 cell cycle progression. Two key substrates of mTORC1 are ribosomal subunit S6 kinase (S6K) and eukaryotic initiation factor 4E (eIF4E) binding protein-1 (4E-BP1). We reported previously that simultaneous knockdown of S6K and eIF4E causes a transforming growth factor-β (TGF-β)-dependent G1 cell cycle arrest in MDA-MB-231 human breast cancer cells. Rapamycin inhibits the phosphorylation of S6K at nano-molar concentrations in MDA-MB-231 cells; however, micro-molar concentrations of rapamycin are required to inhibit phosphorylation of 4E-BP1 - the phosphorylation of which liberates eIF4E to initiate translation. Micro-molar doses of rapamycin are required for complete G1 cell cycle arrest - indicating that 4E-BP1 is a critical target of mTOR for promoting cell cycle progression. Data are provided demonstrating that G1 cell cycle arrest induced by rapamycin is due to up-regulation of TGF-β signaling and down-regulation of Rb phosphorylation via phosphorylation of the mTORC1 substrates S6K and 4E-BP1 respectively. These findings enhance the current understanding of the cytostatic effects of mTORC1 suppression with therapeutic implications.
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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.