Ask about this productRelated genes to: ZIC5 Blocking Peptide
- Gene:
- ZIC5 NIH gene
- Name:
- Zic family member 5
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 13q32.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-30
- Date modifiied:
- 2016-10-05
Related products to: ZIC5 Blocking Peptide
Related articles to: ZIC5 Blocking Peptide
- Oral squamous cell carcinoma (OSCC) commonly arises from oral potentially malignant disorders (OPMDs), yet reliable molecular biomarkers that predict malignant transformation remain scarce. Because epithelial carcinogenesis follows similar multistep trajectories across multiple organs, pan-cancer transcriptional analyses may reveal conserved pathways relevant to early oral tumorigenesis. This study aimed to identify shared transcriptional signatures across carcinomas and evaluate their applicability to precancerous-to-carcinoma progression. Bulk RNA-seq data from five carcinomas (lung, colon, breast, prostate, and head and neck squamous cell carcinoma, HNSCC) were obtained from TCGA to identify shared differentially expressed genes (DEGs) (|logFC| ≥ 2; FDR < 0.05). Functional enrichment, clustering, and gene-pathway network analyses characterized conserved biological processes. Independent GEO datasets containing premalignant and malignant samples, including OPMD and OSCC cohorts, were examined to assess early-stage relevance. A conserved 45-gene signature was identified, enriched for transcriptional regulation, chromatin organization, and RNA polymerase II-mediated processes. Regulatory hubs, including ZIC5, MYBL2, ONECUT2, POU4F1, and PDX1, and strong upregulation of cancer-testis antigens (MAGEA3, MAGEA6, MAGEC2) were notable. Integration with premalignant datasets revealed 13 genes consistently dysregulated across early lesions, involving pathways such as cell differentiation, apoptosis, and lipid transport. Several genes remained altered from normal tissue through OPMD to OSCC, supporting their potential as stable biomarkers. This study identifies conserved transcriptional programs shared across epithelial cancers and detectable in OPMDs. These findings highlight promising biomarker and regulatory candidates for improving early detection and risk stratification of oral precancer, addressing a critical unmet need in OSCC prevention and clinical management. - Source: PubMed
Publication date: 2026/04/13
Kazemi Kimia SadatMiyazawa MartaHanemann João Adolfo CostaIonta MarisaOliveira Pollyanna Francielli deLeask AndrewFranca Cristiane MirandaSperandio Felipe Fornias - piRNAs (PIWI-interacting RNAs) can significantly modify the expression of protein-coding genes by suppressing the translation process. The aim of this work was to computationally evaluate the potential interactions between piRNAs and the mRNA of the gene, as well as other genes involved in key metabolic pathways related to health and lifespan regulation. - Source: PubMed
Publication date: 2026/02/18
Pyrkova AnnaAkhmetova KyrmyzyZhanuzakov MuratTauassarova MakpalRakhmetulina AizhanNiyazova RaigulOrazova SaltanatZielenkiewicz PiotrIvashchenko Anatoliy - Colorectal cancer (CRC), a highly heterogeneous disease, is the second leading cause of cancer related deaths. Mounting evidence has indicated that the zinc finger of the cerebellum 5 (ZIC5) is involved in the pathological processes of cancer. At present, there are few and conflicting studies on ZIC5 in CRC. The aim of this study was to elucidate the clinical value, function and molecular mechanism of ZIC5 in colon cancer. ZIC5 expression analysis in pan-cancer was performed using the TCGA database. The correlation of ZIC5 expression with clinicopathologic parameters of colon cancer was assessed in public and external datasets, respectively. The influence of ZIC5 expression on survival was analyzed by Kaplan-Meier (KM) curve and Cox regression models. In addition, a series of in vitro experiments on cell proliferation, invasion, migration and stemness were performed to further explore the function and potential mechanisms of ZIC5 in colon cancer. ZIC5 mRNA expression is significantly elevated in the vast majority of cancers. We found that ZIC5 is elevated in colon cancer tissues, and high ZIC5 expression was associated with poorer survival of colon cancer patients. ZIC5 expression was positively correlated with the malignant pathological phenotype, and it's an independent risk marker for the overall survival (OS) of colon cancer patients. We demonstrated that ZIC5 promoted proliferation, invasion, migration and EMT of colon cancer cells. Additionally, ZIC5 enhances colon cancer stem cell (CSC) properties. Mechanistically, ZIC5 functions in colon cancer cells by upregulating Wnt signaling. ZIC5 could enhance Wnt/β-catenin signaling by interacting with β-catenin. Interestingly, in HCT116 cells, ZIC5 doesn't affect the protein level of β-catenin and its nuclear translocation likely due to the deletion mutation of β-catenin at Ser45. We identified ZIC5 as a survival marker for colon cancer patients. Our study shows that inhibition of ZIC5 might be a potential therapeutic strategy for colon cancer. - Source: PubMed
Publication date: 2025/11/20
Li XiaopengZhao ChenyeMu MingchaoYuan HangChen GangChen ShihuiHuo XiongweiSun XuejunYu Junhui - This study aims to explore the effects of silencing Zic family member 5 (ZIC5) on glucose metabolism and disulfidptosis in lung adenocarcinoma (LUAD) cells. - Source: PubMed
Publication date: 2025/05/14
Zeng CimeiHuang DenggaoWang LeiLiang HaimeiMa Ximiao - Existing knowledge regarding the involvement of lncRNA OIP5-AS1 in lung adenocarcinoma (LUAD) development is still incomplete and requires further investigation. Our research aimed to reveal the function of OIP5-AS1 in LUAD. We evaluated the level of OIP5-AS1 and its association with clinicopathological factors in LUAD. The research examined the potential implications of targeting OIP5-AS1 in mitigating the invasive properties of lung cancer cells. A nude mouse xenograft model was utilised to examine tumour growth. We used bioinformatics data and a dual-luciferase reporter assay to study the interactions between OIP5-AS1 and hsa-miR-29b-3p. OIP5-AS1 was significantly overexpressed in LUAD, with a higher level correlating with adverse clinicopathological features. Knockdown of OIP5-AS1 resulted in notable decreases in LUAD cell growth, movement, and aggressive behaviour, accompanied by a decrease in tumour size in vivo. Furthermore, OIP5-AS1 was confirmed to act as a molecular sponge for hsa-miR-29b-3p. The elevated expression of hsa-miR-29b-3p intensified the inhibitory outcomes of OIP5-AS1 knockdown on LUAD cell properties. ZIC5 was experimentally determined to be a direct molecular target of hs-miR-29b-3p, emphasising its integral position in the regulatory interaction. This study reveals a new regulatory route involving OIP5-AS1, hsa-miR-29b-3p and ZIC5 in LUAD pathogenesis. Given its oncogenic traits, OIP5-AS1 presents a promising predictive biomarker and therapeutic target for optimising lung cancer treatment. - Source: PubMed
Liang LongLuo YingLi DanyangSun Yongchang