ArticleOncotarget2016
mTORC1-mediated downregulation of COX2 restrains tumor growth caused by TSC2 deficiency.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
The trial behind it
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Synergistic anticancer effects of mitochondria-targeting peptide combined with paclitaxel in breast cancer cells: a preclinical study.Annals of surgical treatment and research · 2025Article
- SLC3A2 promotes tumor-associated macrophage polarization through metabolic reprogramming in lung cancer.Cancer science · 2023Article
- Rise of the natural red pigment 'prodigiosin' as an immunomodulator in cancer.Cancer cell international · 2022Review
- Integrated Pathways of COX-2 and mTOR: Roles in Cell Sensing and Alzheimer's Disease.Frontiers in neuroscience · 2020Review
- COX2 expression is associated with proliferation and tumor extension in vestibular schwannoma but is not influenced by acetylsalicylic acid intake.Acta neuropathologica communications · 2019Article
- A survey of transcriptome complexity in Sus scrofa using single-molecule long-read sequencing.DNA research : an international journal for rapid publication of reports on genes and genomes · 2018Article
- mTOR Signaling and Neural Stem Cells: The Tuberous Sclerosis Complex Model.International journal of molecular sciences · 2018Review
- Hyperactivated mTORC1 downregulation of FOXO3a/PDGFRα/AKT cascade restrains tuberous sclerosis complex-associated tumor development.Oncotarget · 2017Article
- Long-term outcomes of epilepsy surgery in tuberous sclerosis complex.Journal of neurology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tuberous sclerosis complex (TSC), caused by loss-of-function mutations in the TSC1 or TSC2 gene, is characterized by benign tumor formation in multiple organs. Hyperactivation of mammalian target of rapamycin complex 1 (mTORC1) is the primary alteration underlying TSC tumors. By analyzing Tsc2-null mouse embryonic fibroblasts (MEFs) and rat uterine leiomyoma-derived Tsc2-null ELT3 cells, we detected evidence for the involvement of cyclooxygenase 2 (COX2) as a downstream target of mTORC1 in the development of TSC tumors. We showed that loss of TSC2 led to decreased COX2 expression through activation of an mTORC1/signal transducer and activator of transcription 3 (STAT3) signaling pathway. Overexpression of COX2 promoted proliferation and tumoral growth of Tsc2-null cells. COX2 knockdown inhibited the proliferation of the control cells. COX2 enhanced Tsc2-null cell growth through upregulation of interleukin-6 (IL-6). In addition, rapamycin in combination with celecoxib, a COX2 inhibitor, strongly inhibited Tsc2-deficient cell growth. We conclude that downregulation of COX2 exerts a protective effect against hyperactivated mTORC1-mediated tumorigenesis caused by the loss of TSC2, and the combination of rapamycin and celecoxib may be an effective new approach to treating TSC.
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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.