BTBD10 inhibits glioma tumorigenesis by downregulating cyclin D1 and p-Akt
The aim of this study was to investigate the role of BTBD10 in glioma tumorigenesis. The mRNA and protein levels of BTBD10 in 52 glioma tissues and eight normal brain tissues were determined using reverse transcription polymerase chain reaction (RT-PCR) and western blot analysis, respectively. U251...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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De Gruyter
2022-08-01
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| Series: | Open Life Sciences |
| Subjects: | |
| Online Access: | https://doi.org/10.1515/biol-2022-0103 |
| _version_ | 1828108144104964096 |
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| author | Liu Yu Li Sen Chen Ruoping Chen Juxiang Xiao Bo Lu Yicheng Liu Jiangang |
| author_facet | Liu Yu Li Sen Chen Ruoping Chen Juxiang Xiao Bo Lu Yicheng Liu Jiangang |
| author_sort | Liu Yu |
| collection | DOAJ |
| description | The aim of this study was to investigate the role of BTBD10 in glioma tumorigenesis. The mRNA and protein levels of BTBD10 in 52 glioma tissues and eight normal brain tissues were determined using reverse transcription polymerase chain reaction (RT-PCR) and western blot analysis, respectively. U251 human glioblastoma cells were infected with BTBD10-expressing or control lentiviruses. Cell growth was evaluated using the methyl thiazolyl tetrazolium (MTT) assay. Cell apoptosis and cell cycle distribution were analyzed using flow cytometry. Cyclin D1 and p-Akt levels were determined using western blot analysis. The results showed that BTBD10 mRNA and protein levels were significantly lower in glioma tissues than in normal brain tissues. Additionally, BTBD10 levels were significantly lower in high-grade gliomas than in low-grade tumors. Compared with control cells, U251 cells overexpressing BTBD10 exhibited decreased cell proliferation, increased cell accumulation at the G0/G1 phase, increased cell apoptosis, and decreased levels of cyclin D1 and p-Akt. These findings show that BTBD10 is downregulated in human glioma tissue and that BTBD10 expression negatively correlates with the pathological grade of the tumor. Furthermore, BTBD10 overexpression inhibits proliferation, induces G0/G1 arrest, and promotes apoptosis in human glioblastoma cells by downregulating cyclin D1- and Akt-dependent signaling pathways. |
| first_indexed | 2024-04-11T10:43:13Z |
| format | Article |
| id | doaj.art-52f14ac72e7341f29ace50f8add562a3 |
| institution | Directory Open Access Journal |
| issn | 2391-5412 |
| language | English |
| last_indexed | 2024-04-11T10:43:13Z |
| publishDate | 2022-08-01 |
| publisher | De Gruyter |
| record_format | Article |
| series | Open Life Sciences |
| spelling | doaj.art-52f14ac72e7341f29ace50f8add562a32022-12-22T04:29:08ZengDe GruyterOpen Life Sciences2391-54122022-08-0117190791610.1515/biol-2022-0103BTBD10 inhibits glioma tumorigenesis by downregulating cyclin D1 and p-AktLiu Yu0Li Sen1Chen Ruoping2Chen Juxiang3Xiao Bo4Lu Yicheng5Liu Jiangang6Department of Neurosurgery, Shanghai Children’s Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200000, ChinaDepartment of Neurosurgery, Shanghai Children’s Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200000, ChinaDepartment of Neurosurgery, Shanghai Children’s Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200000, ChinaDepartment of Neurosurgery, Shanghai Changzheng Hospital, Shanghai, 200000, ChinaDepartment of Neurosurgery, Shanghai Children’s Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200000, ChinaDepartment of Neurosurgery, Shanghai Changzheng Hospital, Shanghai, 200000, ChinaDepartment of Neurosurgery, Shanghai Children’s Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200000, ChinaThe aim of this study was to investigate the role of BTBD10 in glioma tumorigenesis. The mRNA and protein levels of BTBD10 in 52 glioma tissues and eight normal brain tissues were determined using reverse transcription polymerase chain reaction (RT-PCR) and western blot analysis, respectively. U251 human glioblastoma cells were infected with BTBD10-expressing or control lentiviruses. Cell growth was evaluated using the methyl thiazolyl tetrazolium (MTT) assay. Cell apoptosis and cell cycle distribution were analyzed using flow cytometry. Cyclin D1 and p-Akt levels were determined using western blot analysis. The results showed that BTBD10 mRNA and protein levels were significantly lower in glioma tissues than in normal brain tissues. Additionally, BTBD10 levels were significantly lower in high-grade gliomas than in low-grade tumors. Compared with control cells, U251 cells overexpressing BTBD10 exhibited decreased cell proliferation, increased cell accumulation at the G0/G1 phase, increased cell apoptosis, and decreased levels of cyclin D1 and p-Akt. These findings show that BTBD10 is downregulated in human glioma tissue and that BTBD10 expression negatively correlates with the pathological grade of the tumor. Furthermore, BTBD10 overexpression inhibits proliferation, induces G0/G1 arrest, and promotes apoptosis in human glioblastoma cells by downregulating cyclin D1- and Akt-dependent signaling pathways.https://doi.org/10.1515/biol-2022-0103gliomabtbd10proliferationapoptosiscyclin d1akt |
| spellingShingle | Liu Yu Li Sen Chen Ruoping Chen Juxiang Xiao Bo Lu Yicheng Liu Jiangang BTBD10 inhibits glioma tumorigenesis by downregulating cyclin D1 and p-Akt Open Life Sciences glioma btbd10 proliferation apoptosis cyclin d1 akt |
| title | BTBD10 inhibits glioma tumorigenesis by downregulating cyclin D1 and p-Akt |
| title_full | BTBD10 inhibits glioma tumorigenesis by downregulating cyclin D1 and p-Akt |
| title_fullStr | BTBD10 inhibits glioma tumorigenesis by downregulating cyclin D1 and p-Akt |
| title_full_unstemmed | BTBD10 inhibits glioma tumorigenesis by downregulating cyclin D1 and p-Akt |
| title_short | BTBD10 inhibits glioma tumorigenesis by downregulating cyclin D1 and p-Akt |
| title_sort | btbd10 inhibits glioma tumorigenesis by downregulating cyclin d1 and p akt |
| topic | glioma btbd10 proliferation apoptosis cyclin d1 akt |
| url | https://doi.org/10.1515/biol-2022-0103 |
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