SLC38A5 suppresses ferroptosis through glutamine-mediated activation of the PI3K/AKT/mTOR signaling in osteosarcoma
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View abstract on PubMed
Summary
This summary is machine-generated.Solute carrier family 38 member 5 (SLC38A5) promotes osteosarcoma growth by enhancing cell proliferation, migration, and invasion. Targeting SLC38A5 and the PI3K/AKT pathway offers a potential therapeutic strategy for osteosarcoma.
Area Of Science
- Oncology
- Molecular Biology
- Biochemistry
Background
- Solute carrier family 38 member 5 (SLC38A5) is an amino acid transporter implicated in cellular processes.
- Its role in osteosarcoma progression and underlying mechanisms remain largely uncharacterized.
Purpose Of The Study
- To investigate the dysregulation and prognostic value of SLC38A5 in osteosarcoma.
- To elucidate the functional role and molecular mechanisms of SLC38A5 in osteosarcoma progression.
Main Methods
- Database analysis and in vitro assays (CCK-8, colony formation, migration, invasion).
- Western blot, metabolic assays, and in vivo xenograft models in nude mice.
- Exploration of downstream signaling pathways including PI3K/AKT/mTOR and SREBP1/SCD-1.
Main Results
- SLC38A5 is upregulated in osteosarcoma, correlating with poor patient prognosis.
- SLC38A5 overexpression enhances osteosarcoma cell proliferation, migration, and invasion; PI3K inhibition counteracts these effects.
- Silencing SLC38A5 inhibits tumor growth in vivo; SLC38A5 transports glutamine, activating PI3K/AKT/mTOR and SREBP1/SCD-1 pathways, suppressing ferroptosis.
Conclusions
- SLC38A5 promotes osteosarcoma progression through glutamine-mediated PI3K/AKT/mTOR signaling, inhibiting ferroptosis.
- Targeting SLC38A5 and the PI3K/AKT pathway presents a promising therapeutic avenue for osteosarcoma treatment.
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