CBX3 promotes clear cell renal carcinoma through PI3K/AKT activation and aberrant immunity

Chen, Jiasheng; Lin, Yuxin; zheng, Shukai; Chen, Qingshan; Tang, Shijie; Zhong, Xiaoping

doi:10.1186/s12967-023-04478-9

Cited by 5 publications

(1 citation statement)

References 62 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The Gene Ontology (GO) database (http://www.geneontology.org) integrates biological model databases and other research ndings to analyze vast amounts of genetic information in terms of cellular components (CCs), molecular functions (MFs), and biological processes (BPs) [25]. The Kyoto Encyclopedia of Genes and Genomes (KEGG, https://www.genome.jp/kegg/) is a comprehensive database for systematic gene function analysis that encompasses the latest gene function annotations [26].…”

Section: Go Analysis and Kegg Pathway Enrichment Analysismentioning

confidence: 99%

Posttraumatic stress disorder is a risk factor for migraine: two-sample Mendelian randomization and bioinformatic analysis

Li,

Wang,

Cao

et al. 2024

Preprint

View full text Add to dashboard Cite

Background The association between posttraumatic stress disorder (PTSD) and migraine is a matter of particular concern in clinical practice. Migraine can manifest as the initial somatic symptom of PTSD, one of its sequelae, or even serve as a significant obstacle to effectively treating PTSD. Additionally, individuals with migraines are more susceptible to developing PTSD. Consequently, this study employed bidirectional Mendelian randomization (MR) analysis to investigate the causal relationship between PTSD and migraine while utilizing bioinformatics to analyze their mechanistic connection. Methods We identified single-nucleotide polymorphisms (SNPs) associated with migraine and PTSD through genome-wide association studies (GWASs) conducted by independent consortia. Then, we used these SNPs as instrumental variables to estimate the causal effects of migraine on PTSD and vice versa. MR analysis was performed using the inverse-variance weighted (IVW) method. The MR‒Egger method and the weighted median method were employed to assess the robustness of the findings. Additionally, disease targets associated with both PSTD and migraine were identified by searching the DisGeNET and OMIM databases. The Venny 2.1 software tool was utilized to determine the intersections among these targets, which were then imported into the STRING database for constructing a PPI network. Subsequently, the Cytoscape 3.7 software tool was used for visualization and analysis of the network. Furthermore, common targets were imported into Metascape for Gene Ontology (GO) and KEGG pathway enrichment analysis. Results MR analysis revealed a substantial causal association between PTSD and migraine;however, currently, there is no definitive causal link established between aura migraines or nonaura migraines and PTSD. A total of 107 targets were found to be common to both PTSD and migraine patients. Subsequently, a PPI network comprising 92 nodes connected by 845 edges was constructed based on these shared disease targets. Enrichment analysis revealed their involvement in various BPs, CCs, and MFs. Additionally, the analysis indicated their association with 12 KEGG signaling pathways. Conclusion These results revealed a causal relationship between PTSD and migraine and suggested that further investigations into the mechanisms and specific targets involved in PTSD and migraine should focus particularly on aspects such as neurodegenerative changes, inflammation and the CAMP pathway.

show abstract

Section: Go Analysis and Kegg Pathway Enrichment Analysismentioning

confidence: 99%

Posttraumatic stress disorder is a risk factor for migraine: two-sample Mendelian randomization and bioinformatic analysis

Li,

Wang,

Cao

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

CBX3 Downregulates HLTF to Activate PI3K/AKT Signaling Promoting Cholangiocarcinoma

Xie,

Liang,

Mao

et al. 2024

Advanced Biology

View full text Add to dashboard Cite

Cholangiocarcinoma (CCA) is an aggressive cancer with poor response to chemotherapy or radiation, necessitating novel therapeutic approaches. Epigenetic regulation, which is reversible, plays a significant role in cancer progression. CBX3 (HP1γ), a key heterochromatin protein, regulates gene expression by interacting with histone H3 lysine 9 trimethyl (H3K9me3) markers. While CBX3 is linked to tumor progression in various cancers, its role in CCA remains unclear. This study reveals that CBX3 and H3K9me3 enrich the HLTF promoter, a gene involved in chromatin remodeling and DNA repair. HLTF is often inactivated by hypermethylation in other cancers, suggesting tumor‐suppressive properties. Depleting CBX3 in CCA cells elevates HLTF expression, reducing proliferation, while HLTF silencing reverses this effect. Furthermore, HLTF overexpression inhibits PI3K‐AKT signaling activated by CBX3. These findings suggest CBX3 promotes CCA progression by suppressing HLTF expression.

show abstract

The role of BUD31 in clear cell renal cell carcinoma: prognostic significance, alternative splicing, and tumor immune environment

Wu,

Fan,

Zhang

et al. 2024

Clin Exp Med

View full text Add to dashboard Cite

BUD31, a splicing factor, is linked to various cancers. This study examines BUD31's expression, prognostic value, mutation profile, genomic instability, tumor immune environment, and role in clear cell renal cell carcinoma (ccRCC), focusing on cell cycle regulation via alternative splicing. BUD31 expression was analyzed using TCGA and GTEx databases across 33 cancers. Techniques included IHC staining, survival analysis, Cox regression, and nomogram construction. Mutation landscape, genomic instability, and tumor immune microenvironment were evaluated. Functional assays on ccRCC cell lines involved BUD31 knockdown, RNA sequencing, and alternative splicing analysis. BUD31 was upregulated in multiple tumors, including ccRCC. High BUD31 expression correlated with worse survival outcomes and was identified as an independent predictor of poor prognosis in ccRCC. High BUD31 expression also correlated with increased genomic instability and a less active immune microenvironment. BUD31 knockdown inhibited cell proliferation, migration, and invasion in vitro and reduced tumor growth in vivo. RNA sequencing identified 390 alternative splicing events regulated by BUD31, including 17 cell cycle-related genes. KEGG analysis highlighted pathways involved in cell cycle regulation, indicating BUD31's role in promoting cell cycle progression through alternative splicing. BUD31 is upregulated in various tumors and is associated with poor outcomes, increased genomic instability, and a suppressed immune microenvironment in ccRCC. BUD31 promotes cell cycle progression via alternative splicing, suggesting it as a prognostic biomarker and potential therapeutic target in ccRCC. Supplementary Information The online version contains supplementary material available at 10.1007/s10238-024-01451-8.

show abstract

CBX3 promotes clear cell renal carcinoma through PI3K/AKT activation and aberrant immunity

Cited by 5 publications

References 62 publications

Posttraumatic stress disorder is a risk factor for migraine: two-sample Mendelian randomization and bioinformatic analysis

Posttraumatic stress disorder is a risk factor for migraine: two-sample Mendelian randomization and bioinformatic analysis

CBX3 Downregulates HLTF to Activate PI3K/AKT Signaling Promoting Cholangiocarcinoma

The role of BUD31 in clear cell renal cell carcinoma: prognostic significance, alternative splicing, and tumor immune environment

Contact Info

Product

Resources

About