ArticleThe Journal of clinical investigation2019
Lkb1 deletion in periosteal mesenchymal progenitors induces osteogenic tumors through mTORC1 activation.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 49 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
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
49 citing papers in PubMed, 73 citations in OpenAlex.
- Article
- Fibrous-layer resident Angptl7Cell research · 2026Article
- The Periosteum in Health and Disease.Current osteoporosis reports · 2025Review
- Cathepsin K inhibition promotes efficient differentiation of human embryonic stem cells to mature cardiomyocytes by mediating glucolipid metabolism and cellular energy homeostasis.Stem cell research & therapy · 2025Article
- Apolipoprotein E is a marker of all chondrocytes in the growth plate resting zone.Bone research · 2025Article
- Insights into targeting LKB1 in tumorigenesis.Genes & diseases · 2025Review
- Identification and function of periosteal skeletal stem cells in skeletal development, homeostasis, and disease.Journal of orthopaedic translation · 2025Review
- Nuclear farnesoid X receptor protects against bone loss by driving osteoblast differentiation through stabilizing RUNX2.Bone research · 2025Article
- Signaling pathway mechanisms of circadian clock gene Bmal1 regulating bone and cartilage metabolism: a review.Bone research · 2025Review
- Pre-clinical Murine Models of Bone Sarcomas.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Cathepsin K-Positive Cell Lineage Promotes In Situ Dentin Formation Controlled by Nociceptive Sonic Hedgehog.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The Hippo signalling pathway in bone homeostasis: Under the regulation of mechanics and aging.Cell proliferation · 2024Review
- Itm2a expression marks periosteal skeletal stem cells that contribute to bone fracture healing.The Journal of clinical investigation · 2024Article
- Apolipoprotein E is a novel marker for chondrocytes in the growth plate resting zone.Research square · 2024Article
- Skeletal stem cells in bone development, homeostasis, and disease.Protein & cell · 2024Review
- MicroRNAs targeted mTOR as therapeutic agents to improve radiotherapy outcome.Cancer cell international · 2024Review
- Periosteum Containing Implicit Stem Cells: A Progressive Source of Inspiration for Bone Tissue Regeneration.International journal of molecular sciences · 2024Review
- Identifying squalene epoxidase as a metabolic vulnerability in high-risk osteosarcoma using an artificial intelligence-derived prognostic index.Clinical and translational medicine · 2024Article
- Discovery of CTSK+ Periosteal Stem Cells Mediating Bone Repair in Orbital Reconstruction.Investigative ophthalmology & visual science · 2023Article
- Review
Corrections and comments
- Retracted
Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone osteogenic sarcoma has a poor prognosis as the exact cell of origin and the signaling pathways underling tumor formation remain undefined. Here, we report an osteogenic tumor mouse model based on the conditional knockout of liver kinase b1 (Lkb1; also known as Stk11) in Cathepsin K (Ctsk)-Cre expressing cells. Lineage tracing studies demonstrated that Ctsk-Cre could label a population of periosteal cells. The cells functioned as mesenchymal progenitors with regard to markers and functional properties. LKB1 deficiency increased proliferation and osteoblast differentiation of Ctsk+ periosteal cells, while downregulation of mTORC1 activity, using Raptor genetic mouse model or mTORC1 inhibitor treatment, ameliorated tumor progression of Ctsk-Cre Lkb1fllfl mice. Xenograft mouse models, using human osteosarcoma cell lines, also demonstrated that LKB1 deficiency promoted tumor formation, while mTOR inhibition suppressed xenograft tumor growth. In summary, we identified periosteum-derived Ctsk-Cre expressing cells as a cell of origin for osteogenic tumor and suggested the LKB1-mTORC1 pathway as a promising target for treatment of osteogenic tumor.
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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 Socratic graph.