Article ; Online: Prognosis-related VDAC1 regulates the proliferation and apoptosis of osteosarcoma cells via the MAPK signaling pathway.
2023 Volume 115, Issue 3, Page(s) 110595
Abstract: The role of VDAC1 in osteosarcoma is unclear. We explored the effect of VDAC1 on osteosarcoma development by combining bioinformatic analysis and experimental identification. This study suggested that VDAC1 is an independent prognostic factor for ... ...
Abstract | The role of VDAC1 in osteosarcoma is unclear. We explored the effect of VDAC1 on osteosarcoma development by combining bioinformatic analysis and experimental identification. This study suggested that VDAC1 is an independent prognostic factor for osteosarcoma. Patients with high VDAC1 expression have a poor survival rate. VDAC1 was overexpressed in osteosarcoma cells. After silencing VDAC1, the proliferation of osteosarcoma cells decreased, and the apoptosis rate increased. Gene set variation analysis and gene set enrichment analysis indicated that VDAC1 was associated with the MAPK signaling pathway. After VDAC1 siRNA, SB203580 (a p38 inhibitor), SP600125 (a JNK inhibitor) and α-pifithrin (a p53 inhibitor) treatment, the proliferative capacity was weaker in the si-VDAC1 group than in the si-VDAC1 + SB203580, si-VDAC1 + SP600125, and si-VDAC1 + α-pifithrin groups. In conclusion, prognosis-related VDAC1 can affect osteosarcoma cells' proliferative activity and apoptosis level. The MAPK signaling pathway mediates VDAC1 regulation of osteosarcoma cell development. |
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MeSH term(s) | Humans ; Cell Line, Tumor ; Signal Transduction ; Osteosarcoma/genetics ; Apoptosis/genetics ; Bone Neoplasms/genetics ; Cell Proliferation/genetics ; Prognosis ; Voltage-Dependent Anion Channel 1/metabolism |
Chemical Substances | pyrazolanthrone (1TW30Y2766) ; pifithrin (D213B92S1Y) ; VDAC1 protein, human ; Voltage-Dependent Anion Channel 1 (EC 1.6.-) |
Language | English |
Publishing date | 2023-03-05 |
Publishing country | United States |
Document type | Journal Article |
ZDB-ID | 356334-0 |
ISSN | 1089-8646 ; 0888-7543 |
ISSN (online) | 1089-8646 |
ISSN | 0888-7543 |
DOI | 10.1016/j.ygeno.2023.110595 |
Database | MEDical Literature Analysis and Retrieval System OnLINE |
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