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Solute carrier family 35 member A2 regulates mitophagy through the PI3K/AKT/mTOR axis, promoting the proliferation, migration, and invasion of osteosarcoma cells.
Luo, Xiaohui; Zhang, Jiongfeng; Guo, Chong; Jiang, Ning; Zhang, Feifei; Jiao, Quahui; Xu, Kai; Yang, Jun; Qu, Gaoyang; Lv, Xiao-Bin; Zhang, Zhiping.
Afiliación
  • Luo X; Jiangxi Key Laboratory of Cancer Metastasis and Precision Treatment, The first hospital of Nanchang, The Third Affiliated Hospital of Nanchang University, Jiangxi Medical College, Nanchang University, Nanchang, China; Department of Orthopedics, The first hospital of Nanchang, The Third Affiliated Ho
  • Zhang J; Jiangxi Key Laboratory of Cancer Metastasis and Precision Treatment, The first hospital of Nanchang, The Third Affiliated Hospital of Nanchang University, Jiangxi Medical College, Nanchang University, Nanchang, China; Department of Orthopedics, The first hospital of Nanchang, The Third Affiliated Ho
  • Guo C; Jiangxi Key Laboratory of Cancer Metastasis and Precision Treatment, The first hospital of Nanchang, The Third Affiliated Hospital of Nanchang University, Jiangxi Medical College, Nanchang University, Nanchang, China; Department of Orthopedics, The first hospital of Nanchang, The Third Affiliated Ho
  • Jiang N; Institute of Integrative Medicine, Dalian Medical University, Dalian, Liaoning, China.
  • Zhang F; Jiangxi Key Laboratory of Cancer Metastasis and Precision Treatment, The first hospital of Nanchang, The Third Affiliated Hospital of Nanchang University, Jiangxi Medical College, Nanchang University, Nanchang, China.
  • Jiao Q; Jiangxi Key Laboratory of Cancer Metastasis and Precision Treatment, The first hospital of Nanchang, The Third Affiliated Hospital of Nanchang University, Jiangxi Medical College, Nanchang University, Nanchang, China.
  • Xu K; Jiangxi Key Laboratory of Cancer Metastasis and Precision Treatment, The first hospital of Nanchang, The Third Affiliated Hospital of Nanchang University, Jiangxi Medical College, Nanchang University, Nanchang, China; Department of Orthopedics, The first hospital of Nanchang, The Third Affiliated Ho
  • Yang J; Jiangxi Key Laboratory of Cancer Metastasis and Precision Treatment, The first hospital of Nanchang, The Third Affiliated Hospital of Nanchang University, Jiangxi Medical College, Nanchang University, Nanchang, China.
  • Qu G; Jiangxi Key Laboratory of Cancer Metastasis and Precision Treatment, The first hospital of Nanchang, The Third Affiliated Hospital of Nanchang University, Jiangxi Medical College, Nanchang University, Nanchang, China; Department of Orthopedics, The first hospital of Nanchang, The Third Affiliated Ho
  • Lv XB; Jiangxi Key Laboratory of Cancer Metastasis and Precision Treatment, The first hospital of Nanchang, The Third Affiliated Hospital of Nanchang University, Jiangxi Medical College, Nanchang University, Nanchang, China. Electronic address: nclvxiaobin@sina.cn.
  • Zhang Z; Jiangxi Key Laboratory of Cancer Metastasis and Precision Treatment, The first hospital of Nanchang, The Third Affiliated Hospital of Nanchang University, Jiangxi Medical College, Nanchang University, Nanchang, China; Department of Orthopedics, The first hospital of Nanchang, The Third Affiliated Ho
Gene ; 898: 148110, 2024 Mar 10.
Article en En | MEDLINE | ID: mdl-38151177
ABSTRACT
The treatment of osteosarcoma patients exhibits individual variability, underscoring the critical importance of targeted therapy. Although (Solute carrier family 35 member A2) SLC35A2's role in the progression of various cancers has been extensively investigated, its specific implications in osteosarcoma remain unexplored. Leveraging data from the (The Cancer Genome Atlas) TCGA and (Genotype-Tissue Expression) GTEx databases, we have discerned that SLC35A2 is notably upregulated in osteosarcoma and correlates with the prognosis of osteosarcoma patients. Consequently, it becomes imperative to delve into the role of SLC35A2 in the context of osteosarcoma. Our research substantiates that SLC35A2 exerts a notable influence on mitochondrial autophagy in osteosarcoma, thereby exerting cascading effects on the proliferation, migration, invasion, and apoptosis of osteosarcoma cells. Mechanistically, SLC35A2 orchestrates mitochondrial autophagy via the PI3K/AKT/mTOR signaling pathway. Moreover, we have conducted rigorous animal experiments to further corroborate the repercussions of SLC35A2 on osteosarcoma growth. In summation, our study elucidates that SLC35A2's modulation of mitochondrial autophagy through the PI3K/AKT/mTOR signaling pathway constitutes a pivotal factor in the malignant progression of osteosarcoma, unveiling promising therapeutic targets for patients grappling with this condition.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Óseas / Osteosarcoma Límite: Animals / Humans Idioma: En Revista: Gene Año: 2024 Tipo del documento: Article Pais de publicación: Países Bajos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Óseas / Osteosarcoma Límite: Animals / Humans Idioma: En Revista: Gene Año: 2024 Tipo del documento: Article Pais de publicación: Países Bajos