Ask about this productRelated genes to: ZCCHC12 Blocking Peptide
- Gene:
- ZCCHC12 NIH gene
- Name:
- zinc finger CCHC-type containing 12
- Previous symbol:
- -
- Synonyms:
- FLJ16123, SIZN, SIZN1, PNMA7A
- Chromosome:
- Xq24
- Locus Type:
- gene with protein product
- Date approved:
- 2004-07-14
- Date modifiied:
- 2016-02-12
Related products to: ZCCHC12 Blocking Peptide
Related articles to: ZCCHC12 Blocking Peptide
- Considerable evidence highlights the intricate association between liquid-liquid phase separation (LLPS) and tumorigenesis, progression, and therapy resistance. However, there has been limited exploration of the role of LLPS in hepatoblastoma (HB). This study integrates machine learning techniques with single-cell RNA sequencing (scRNA-seq) to systematically analyze the molecular features of LLPS-associated genes in HB and establish the first LLPS-based prognostic prediction model for HB. - Source: PubMed
Publication date: 2025/07/06
Cai D QCai DianKuiZhao ZhenZheng ZehaoJian ZhixiangShi MudeChen YajinChen JuemingLin Ye - Thyroid cancer (THCA) is a prevalent malignancy of the head and neck region, yet the mechanisms underlying its tumorigenesis and metastasis remain poorly understood. Given that Rho GTPase activating protein 36 (ARHGAP36) has been implicated in various cellular processes related to cancer progression, including cell migration and invasion, it represents a promising candidate for further investigation in THCA. To investigate the gene expression differences in ARHGAP36 between tumor and normal tissues, the GEPIA and UALCAN databases were utilized. Various factors were also evaluated, including sample types, cancer stages, demographics, histological characteristics and nodal status. The LinkedOmics database was used to constructed a co-expression network for ARHGAP36 in THCA. Gene Ontology (GO) process enrichment analysis for ARHGAP36-associated genes was conducted via Metascape. The TIMER and TISCH databases were employed to explore the relationships between ARHGAP36 and immune markers as well as cell clusters. Functional assays were performed to assess cellular behaviors such as proliferation, migration and apoptosis. The results indicated that ARHGAP36 expression was significantly elevated in THCA tissues compared with normal tissues. Co-expression analysis revealed significant links between ARHGAP36 and key genes, including IGSF1, DPYSL3, ZCCHC12, CD97, LOXL4, CST2 and WSCD. The enriched GO processes involved T-cell immunity, particularly highlighting the association between ARHGAP36 and CD4 T cell infiltration. Notably, the downregulation of ARHGAP36 reduced tumor cell proliferation, migration and invasion while enhancing apoptosis. In conclusion, the findings of the present study indicate that ARHGAP36 plays a crucial role in facilitating immune evasion and promoting THCA progression. This underscores its potential as a diagnostic marker and therapeutic target in THCA. - Source: PubMed
Publication date: 2025/06/12
Yang LiyunLiu JunzhiGao YuhuanHuang ShuixianWu Geping - Local recurrence and distal metastasis negatively impact the survival and quality of life in patients with papillary thyroid cancer (PTC). Therefore, identifying potential biomarkers and therapeutic targets for PTC is clinically crucial. In this study, we performed a multiomics analysis that identified a subset of CD36+ proinflammatory macrophages within the tumor microenvironment of PTC. The recruitment of CD36+ macrophages to premalignant regions strongly correlated with unfavorable outcomes in PTC, and the presence of tumor-infiltrating CD36+ macrophages was determined to be a risk factor for recurrence. The CD36+ macrophages exhibited interactions with metabolically active ZCCHC12+ tumor cells. By secreting SPP1, the CD36+ macrophages activated the PI3K-AKT signaling pathway, thereby promoting proliferation of the cancer cells. Dysregulation of iodine metabolism was closely related to the acquisition of the pro-inflammatory phenotype in macrophages. Iodine supplementation inhibited the activation of proinflammatory signaling and impeded the development of CD36+ macrophages by enhancing DUSP2 expression. Overall, our findings shed light on the intricate cross-talk between CD36+ macrophages and ZCCHC12+ tumor cells, providing valuable insights for the treatment and prognosis of PTC. - Source: PubMed
Zhang XinGuo LimeiTian WenyuYang YingYin YueQiu YaruoWang WeixuanLi YangZhang GuangzeZhao XuyangWang GuangxiLin ZhiqiangYang MengZhao WeiLu Dan - The zinc-finger CCHC-type (ZCCHC) superfamily proteins are characterized by the shared sequence CX2-CX4-HX4-C and thought to own high affinity to single-stranded nucleic acids, particularly RNAs. In humans, a total of 24 ZCCHC proteins have been annotated in the HUGO Gene Nomenclature Committee (HGNC, https://www.genenames.org/ ) database with most of these members involved in multiple steps of RNA metabolism. Many studies have indicated that the ZCCHC genes play a regulatory role in the development and progression of solid tumors. To date, the expression pattern and prognostic value of ZCCHC factors in thyroid carcinomas have not been reported. - Source: PubMed
Publication date: 2023/10/17
Yin YinChen JingChen QianHe HongyanZhu NannanXia PengchengYu ChunliMeng Lingyun - The E3 ubiquitin ligase Ube3a is biallelically expressed in neural progenitors and glial cells, suggesting that UBE3A gain-of-function mutations might cause neurodevelopmental disorders irrespective of parent of origin. Here, we engineered a mouse line that harbors an autism-linked UBE3A (T503A in mouse) gain-of-function mutation and evaluated phenotypes in animals that inherited the mutant allele paternally, maternally, or from both parents. We find that paternally and maternally expressed UBE3A results in elevated UBE3A activity in neural progenitors and glial cells. Expression of UBE3A from the maternal allele, but not the paternal one, leads to a persistent elevation of UBE3A activity in neurons. Mutant mice display behavioral phenotypes that differ by parent of origin. Expression of UBE3A, irrespective of its parent of origin, promotes transient embryonic expansion of Zcchc12 lineage interneurons. Phenotypes of Ube3a mice are distinct from Angelman syndrome model mice. Our study has clinical implications for a growing number of disease-linked UBE3A gain-of-function mutations. - Source: PubMed
Publication date: 2023/06/28
Xing LeiSimon Jeremy MPtacek Travis SYi Jason JLoo LipinMao HanqianWolter Justin MMcCoy Eric SParanjape Smita RTaylor-Blake BonnieZylka Mark J