BTBD10 inhibits glioma tumorigenesis by downregulating cyclin D1 and p-Akt

Liu, Yu; Li, Sen; Chen, Ruoping; Chen, Juxiang; Xiao, Bo; Lu, Yao; Liu, Jiangang

doi:10.1515/biol-2022-0103

Cited by 3 publications

(1 citation statement)

References 29 publications

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“…The miRNAs promote the degrading and inhibiting translation of mRNA by interacting with their 5′ and 3′ untranslated region (UTR) sequences. Our results showed that TGFBR1 [ 30 ], SUPT6H [ 31 ], CNOT6L [ 32 ], and BTBD10 [ 33 ], which were reported to participate in the regulation of cell apoptosis and follicular development, may be the key target genes for miR-202-5p to regulate goose GCs. Subsequently, the result of qRT-PCR indicates that miR-202-5p impacted the expression of BTBD10 most significantly.…”

Section: Discussionmentioning

confidence: 99%

MiR-202-5p Regulates Geese Follicular Selection by Targeting BTBD10 to Regulate Granulosa Cell Proliferation and Apoptosis

Ran

Xie

et al. 2023

IJMS

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The regulation of granulosa cells (GCs) proliferation and apoptosis is the key step in follicular selection which determines the egg production performance of poultry. miR-202-5p has been reported to be involved in regulating the proliferation and apoptosis of mammalian ovarian GCs. However, its role in regulating the proliferation and apoptosis of goose GCs is still unknown. In the present study, the GCs of pre-hierarchical follicles (phGCs, 8–10 mm) and those of hierarchical follicles (hGCs, F2–F4) were used to investigate the role of miR-202-5p in cell proliferation and apoptosis during follicle selection. In phGCs and hGCs cultured in vitro, miR-202-5p was found to negatively regulate cell proliferation and positively regulate cell apoptosis. The results of RNA-seq showed that BTB Domain Containing 10 (BTBD10) is predicted to be a key target gene for miR-202-5p to regulate the proliferation and apoptosis of GCs. Furthermore, it is confirmed that miR-202-5p can inhibit BTBD10 expression by targeting its 3′UTR region, and BTBD10 was revealed to promote the proliferation and inhibit the apoptosis of phGCs and hGCs. Additionally, co-transfection with BTBD10 effectively prevented miR-202-5p mimic-induced cell apoptosis and the inhibition of cell proliferation. Meanwhile, miR-202-5p also remarkably inhibited the expression of Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic Subunit Beta (PIK3CB) and AKT Serine/Threonine Kinase 1 (AKT1), while it was significantly restored by BTBD10. Overall, miR-202-5p suppresses the proliferation and promotes the apoptosis of GCs through the downregulation of PIK3CB/AKT1 signaling by targeting BTBD10 during follicular selection. Our study provides a theoretical reference for understanding the molecular mechanism of goose follicular selection, as well as a candidate gene for molecular marker-assisted breeding to improve the geese’ egg production performance.

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Section: Discussionmentioning

confidence: 99%

MiR-202-5p Regulates Geese Follicular Selection by Targeting BTBD10 to Regulate Granulosa Cell Proliferation and Apoptosis

Ran

Xie

et al. 2023

IJMS

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A Pan-cancer Analysis of the Role of the Transmembrane Protein 91(TMEM91) in Human Tumors

Jiang

Song

2023

Preprint

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Transmembrane protein 91(TMEM91) encodes a protein belonging to the transmembrane protein family which mediates many human physiological processes, such as the regulation of cell migration and invasion, and participates in the immune response. At present, research on the TMEM family members focuses mostly on the field of molecular mechanisms, and the role of TMEM91 in tumor cells is still unrecognized. Using data from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases, we can analysis the expression of TMEM91 in various tumors. The Kaplan-Meier method was used for the evaluation of the prognostic significance of TMEM91 in patients with pan-cancer. The dif-ferential expression of TMEM91 in diverse cancers with different clinical characteristics was analyzed with the UALCAN database. TIMER was used to explore how TMEM91 correlates with immune infiltration. The correlations between TMEM91 expression immune checkpoint (ICP), tumor mutational burden (TMB), and microsatellite instability (MSI) in human cancers were analyzed via the SangerBox database. Gene Set Cancer Analysis (GSCA) platform was used to investigate the correlation between TMEM91 expression with Copy number variations (CNV) and methylation. Protein-Protein Interaction analysis was performed in the GeneMANIA database. Gene Ontology and Kyoto Encyclopedia of Genes pathway en-richment analyses were further conducted for exploration of TMEM91 function. According to the finding of this study, downregulated TMEM91 expression was observed in numerous tumor tissues. The low TMEM91 expression group showed poor overall survival (OS) and disease-free survival (DFS). TMEM91 was positively correlated with can-cer-associated fibroblast (CAF), and nature killer T cell (NKT), and negatively correlated with CD4 + T cells, B cells and common lymphoid progenitor (CLP). Here, we show that there is a positive relationship between Contingent Negative Variation (CNV) and expression of TMEM91, whereas the correlation of TMEM91 expression with DNA methylation was nega-tive in all cases. Molecular biology experiments were performed to confirm the tumor pro-moting role of TMEM91 in glioma. Function analysis showed that TMEM91 expres-sion-related genes were mainly enriched in response to type I interferon /regulation of viral genome replication/negative regulation of viral process/movement in host environment. In addition, the association between the expression of TMEM91 and the use of the anticancer drug, sensitive anti-tumor drug based on CellMiner were predicted, such as the anticancer drug AS-703569, Hydroxyurea. Our pan-cancer analysis provides a deep understanding of the functions of TMEM91.TMEM91 may affect the oncogenesis and metastasis in different cancers via mediating the immune infiltrating cells and the degree of methylation. This study sheds new light on the mechanism of TMEM family in cancer.

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Identification of Potential Feature Genes in CRSwNP Using Bioinformatics Analysis and Machine Learning Strategies

Wang,

Xu,

et al. 2024

JIR

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Purpose The pathogenesis of CRSwNP is complex and not yet fully explored, so we aimed to identify the pivotal hub genes and associated pathways of CRSwNP, to facilitate the detection of novel diagnostic or therapeutic targets. Methods Utilizing two CRSwNP sequencing datasets from GEO, differential expression gene analysis, WGCNA, and three machine learning methods (LASSO, RF and SVM-RFE) were applied to screen for hub genes. A diagnostic model was then formulated utilizing hub genes, and the AUC was generated to evaluate the performance of the prognostic model and candidate genes. Hub genes were validated through the validation set and qPCR performed on normal mice and CRSwNP mouse model. Lastly, the ssGSEA algorithm was employed to assess the differences in immune infiltration levels. Results A total of 239 DEGs were identified, with 170 upregulated and 69 downregulated in CRSwNP. Enrichment analysis revealed that these DEGs were primarily enriched in pathways related to nucleocytoplasmic transport and HIF-1 signaling pathway. Data yielded by WGCNA analysis contained 183 DEGs. The application of three machine learning algorithms identified 11 hub genes. Following concurrent validation analysis with the validation set and qPCR performed after establishing the mouse model confirmed the overexpression of BTBD10, ERAP1, GIPC1, and PEX6 in CRSwNP. The examination of immune cell infiltration suggested that the infiltration rate of type 2 T helper cell and memory B cell experienced a decline in the CRSwNP group. Conversely, the infiltration rates of Immature dendritic cell and Effector memory CD8 T cell were positive correlation. Conclusion This study successfully identified and validated BTBD10, ERAP1, GIPC1, and PEX6 as potential novel diagnostic or therapeutic targets for CRSwNP, which offers a fresh perspective and a theoretical foundation for the diagnostic prediction and therapeutic approach to CRSwNP.

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BTBD10 inhibits glioma tumorigenesis by downregulating cyclin D1 and p-Akt

Cited by 3 publications

References 29 publications

MiR-202-5p Regulates Geese Follicular Selection by Targeting BTBD10 to Regulate Granulosa Cell Proliferation and Apoptosis

MiR-202-5p Regulates Geese Follicular Selection by Targeting BTBD10 to Regulate Granulosa Cell Proliferation and Apoptosis

A Pan-cancer Analysis of the Role of the Transmembrane Protein 91(TMEM91) in Human Tumors

Identification of Potential Feature Genes in CRSwNP Using Bioinformatics Analysis and Machine Learning Strategies

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