ArticleScientific reports2017
Opposite feedback from mTORC1 to H-ras and K-ras4B downstream of SREBP1.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Oscillatory ERK Signaling and Morphology Determine Heterogeneity of Breast Cancer Cell Chemotaxis via MEK-ERK and p38-MAPK Signaling Pathways.Bioengineering (Basel, Switzerland) · 2023Article
- Review
- Elaiophylin Is a Potent Hsp90/ Cdc37 Protein Interface Inhibitor with K-Ras Nanocluster Selectivity.Biomolecules · 2021Article
- NRAS is unique among RAS proteins in requiring ICMT for trafficking to the plasma membrane.Life science alliance · 2021Article
- Promotion of cancer cell stemness by Ras.Biochemical Society transactions · 2021Review
- Novel Small Molecule Hsp90/Cdc37 Interface Inhibitors Indirectly Target K-Ras-Signaling.Cancers · 2021Article
- Pre-existing Cell States Control Heterogeneity of Both EGFR and CXCR4 Signaling.Cellular and molecular bioengineering · 2021Article
- FLIM-FRET Analysis of Ras Nanoclustering and Membrane-Anchorage.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Mechanisms of Ras Membrane Organization and Signaling: Ras Rocks Again.Biomolecules · 2020Review
- Article
- Short-term cellular memory tunes the signaling responses of the chemokine receptor CXCR4.Science signaling · 2019Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a major growth factor transducer, Ras is an upstream activator of mTORC1, which further integrates nutrient and energy inputs. To ensure a contextual coupling of cell division via Ras/MAPK-signalling and growth via mTORC1-signalling, feedback loops from one pathway back to the other are required. Here we describe a novel feedback from mTORC1, which oppositely affects oncogenic H-ras- and K-ras-signalling output, and as a consequence stemness properties of tumourigenic cells. Amino acid stimulation of mTORC1 increases the processed form of SREBP1, a major lipidome regulator. We show that modulation of the SREBP1 levels downstream of S6K1 has opposite effects on oncogenic H-ras and K-ras nanoscale membrane organisation, ensuing signalling output and promotion of mammospheres expressing these oncogenes. Our data suggest that modulation of phosphatidic acid, a major target of SREBP1 controlled lipid metabolism, is sufficient to affect H-ras and K-ras oppositely in the membrane. Thus mTORC1 activation increases H-ras-, but decreases K-ras-signalling output in cells transformed with the respective oncogene. Given the different impact of these two Ras isoforms on stemness, our results could have implications for stem cell biology and inhibition of cancer stem cells.
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