ArticleMolecular biotechnology2025
Oncogenic Gene CNOT7 Promotes Progression and Induces Poor Prognosis of Glioma.
Article in Molecular biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- High ORC6 expression is a prognostic indicator of poor survival in glioma patients.Scientific reports · 2025Article
- CNOT7 facilitates radiation resistance in colorectal cancer through TRIM21/XRCC6-mediated non-homologous end joining repair.Cell death & disease · 2025Article
- CCR4-NOT Transcription Complex Subunit 7 (CNOT7) Protein and Leukocyte-Associated Immunoglobulin-like Receptor-1 in Breast Cancer Progression: Clinical Mechanistic Insights and In Silico Therapeutic Potential.International journal of molecular sciences · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
Glioma is the most common malignant brain tumor in the central nervous system with the poor prognosis of patients. The CNOT7 (CCR4-NOT Transcription Complex Subunit 7) is an important functional subunit of CCR4-NOT protein complex that has not been reported in glioma. In this study, we aimed to explore the function of CNOT7 in glioma. The TCGA (The Cancer Genome Atlas) and CGGA (Chinese Glioma Genome Atlas) databases were used for investigating the expression and survival condition of CNOT7 in glioma. The cellular function experiments of qRT-PCR, CCK-8 assays, wound healing assays, and Transwell assays were conducted to verify the function of knockdown CNOT7 in the glioma cell lines DBTRG and U251. Enrichment analysis was used to explore the molecular mechanism of CONT7 in glioma. What is more, the upstream regulation transcription factors of CNOT7 were analyzed based on the ChIP-Atlas and cBioportal (provisional) databases, and verified by the qRT-PCR and luciferase reporter assay. The CNOT7 was highly expressed in glioma and presented the poorer prognosis. The knockdown of CNOT7 inhibited the proliferation, migration, and invasion of glioma cell line, compared to control group. The enrichment analysis revealed that the CNOT7 participated in the development of glioma via G2M checkpoint, E2F targets, IL6-JAK-STAT3, and TNF-α signaling pathways via NF-κB. Besides, it was found that the HDAC2 (Human histone deacetylase-2) contributes to increased CNOT7 expression in glioma. The high-expressed CNOT7 is an oncogene with poor prognosis and participate the progression of glioma.
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