The Role of V-ATPase ATP6V0D1 Subunit in Chemoresistance and Ellipticine-Induced Cytoplasmic Vacuolation in Neuroblastoma Cells

Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00064203%3A_____%2F25%3A10499329" target="_blank" >RIV/00064203:_____/25:10499329 - isvavai.cz</a>
Alternative codes found
RIV/00216208:11130/25:10499329
Result on the web
<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=Pgi6dBb8.O" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=Pgi6dBb8.O</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1080/23723556.2025.2518774" target="_blank" >10.1080/23723556.2025.2518774</a>

Result language
angličtina
Original language name
The Role of V-ATPase ATP6V0D1 Subunit in Chemoresistance and Ellipticine-Induced Cytoplasmic Vacuolation in Neuroblastoma Cells
Original language description
Drug resistance remains a major obstacle in neuroblastoma treatment. Lysosomal sequestration, facilitated by the V-ATPase proton pump, is one of the mechanisms of chemoresistance. Overexpression of the ATP6V0D1 subunit of V-ATPase, previously reported in various cancers, was also observed in ellipticine-resistant neuroblastoma cells in our study. Neuroblastoma cells also exhibited increased lysosomal capacity and vacuolation after ellipticine treatment. Knockdown of ATP6V0D1, but not ATP6V1H, enhanced ellipticine sensitivity, suppressed proliferation and migration, decreased lysosomal uptake, and induced G2/M arrest in neuroblastoma cell lines. Notably, inhibiting another V-ATPase subunit, ATP6V1H, had no effect, highlighting the specific role of ATP6V0D1 in drug resistance. Ellipticine-induced vacuolation, identified as endoplasmic reticulum swelling, lacked evidence of paraptosis. ATP6V0D1 knockdown suppressed this phenomenon, whereas ATP6V1H silencing did not. Our findings underscore the importance of ATP6V0D1 in neuroblastoma and suggest potential therapeutic strategies targeting V-ATPase for overcoming drug resistance.
Czech name
—
Czech description
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Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30205 - Hematology

Project
<a href="/en/project/NW24-03-00101" target="_blank" >NW24-03-00101: KDMs expression profile in childhood cancer- relationship to the course of the disease</a><br>
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Publication year
2025
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

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