Ask about this productRelated genes to: CCT5 Blocking Peptide
- Gene:
- CCT5 NIH gene
- Name:
- chaperonin containing TCP1 subunit 5
- Previous symbol:
- -
- Synonyms:
- KIAA0098
- Chromosome:
- 5p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-29
- Date modifiied:
- 2019-04-23
Related products to: CCT5 Blocking Peptide
Related articles to: CCT5 Blocking Peptide
- While Chaperonin Containing TCP1 Subunit 5 (CCT5) is recognized for its involvement in the oncogenesis and advancement of diverse malignancies, its functional significance within the context of colon adenocarcinoma (COAD) has yet to be elucidated. - Source: PubMed
Publication date: 2026/04/28
Wang BoLiu XinruiLi JianmeiDong HuiFan XingxiuWang RuijunGuo JianpingLi Yifeng - Colorectal cancer (CRC) is a leading cause of cancer-related mortality, and early tumorigenesis is closely associated with mitotic dysregulation and chromosomal instability. To define molecular mechanisms supporting mitotic fidelity during CRC initiation, we combined multi-omics profiling, genetically engineered mouse models, and functional assays to examine the role of the chaperonin subunit CCT5. Transcriptomic and proteomic analyses revealed elevated CCT5 expression in stage I CRC and precancerous lesions, indicating diagnostic relevance. The genetic depletion of CCT5 suppressed epithelial proliferation, reduced dysplastic transformation, and limited tumor initiation . In CRC cells, CCT5 silencing impaired proliferation and induced G2/M arrest. Mechanistically, CCT5 interacts with CDC20 and facilitates turnover of the MCC-CDC20-APC/C complex, enabling metaphase-to-anaphase progression. These findings position CCT5 as a regulator of early CRC development with implications for early detection and therapeutic intervention. - Source: PubMed
Publication date: 2026/03/04
Ji MeijunZhuang WenhanGuo YuminXu PengfeiZhou XiaoluLong YanGeng XiaogeJing JiyongZhou XuelongPan WenshengZhang Chenjing - Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide, with cellular senescence playing a context-dependent role in tumor progression and the immunosuppressive microenvironment. This study is aimed at identifying senescence-related gene signatures through integrated single-cell and transcriptomic analyses to construct a robust prognostic model for predicting survival and immunotherapy response in HCC patients. - Source: PubMed
Publication date: 2026/02/10
Yu KaiChen MinqiHou WanchaoLu JinhuaLiu QianhanZeng WanrongDu ZhengcaiHou XiaotaoHao ErweiDeng JiagangGong Peipei - CCT5, a subunit of the chaperonin-containing TCP1 complex, has been implicated in the development of various malignancies. However, its role in bladder cancer remains undefined. This study investigated the functional contribution of CCT5 and its association with Hippo/YAP signaling. Using data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), CCT5 expression and its prognostic significance were analyzed. Single-cell and spatial transcriptomics were employed to explore expression patterns and cellular heterogeneity. Functional assessments were conducted and using xenografts. To elucidate the underlying mechanisms, RNA-seq was integrated with Western blotting analysis. CCT5 was found to be upregulated in bladder cancer and correlated with poor prognosis and aggressive pathological features. Single-cell and spatial analyses revealed that CCT5 was enriched in malignant epithelial subpopulations with high CNV scores, activated oncogenic pathways, and extensive cell-cell interactions. Functionally, CCT5 promoted proliferation, migration, invasion, and G1/S transition while inhibiting apoptosis; its depletion reduced xenograft growth. At the signaling level, CCT5 knockdown enhanced phosphorylation of MST1, LATS1, and YAP, without significant changes in total protein levels, suggesting activation of Hippo/YAP signaling. These findings highlight CCT5 as an oncogenic factor in bladder cancer, potentially acting through the regulation of Hippo/YAP signaling, and propose its potential as a biomarker and therapeutic target in bladder cancer. - Source: PubMed
Publication date: 2026/01/15
Zhang XiaojunFu YuqiangDu YuelinXiong WeiWang JienengZhang HelinLuo YaoZhao YanzongShang Panfeng - Dioxin has emerged as a major and modifiable determinant of tumor burden worldwide. Building on this premise, we investigated whether dioxin-interacting genes (DIGs) are connected to diffuse large B-cell lymphoma (DLBCL) and sought genes that might function as molecular bridges between exposure and clinical outcome. - Source: PubMed
Publication date: 2026/01/16
Chen CanLi YiweiLi YunQian Shenxian