Ask about this productRelated genes to: CHCHD1 Blocking Peptide
- Gene:
- CHCHD1 NIH gene
- Name:
- coiled-coil-helix-coiled-coil-helix domain containing 1
- Previous symbol:
- C10orf34
- Synonyms:
- FLJ25854
- Chromosome:
- 10q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-30
- Date modifiied:
- 2017-07-06
Related products to: CHCHD1 Blocking Peptide
Related articles to: CHCHD1 Blocking Peptide
- The interplay between mitochondrial dysfunction and immune infiltration in heart failure with preserved ejection fraction (HFpEF) remains poorly understood. This study aimed to elucidate this relationship and identify key regulatory genes. - Source: PubMed
Xie YingyingHe HaomingLi YikeChen QiangGao YanxiangZheng Jingang - Coiled-coil-helix-coiled-coil-helix domain containing 1 (CHCHD1) is a mitochondrial protein involved in oxidative phosphorylation and mitochondrial protein synthesis. While its functions have been explored in basic mitochondrial biology, the role of this process in hepatocellular carcinoma (HCC) remains poorly understood. We performed transcriptomic analysis on 272 HCC and 50 normal liver tissue samples to assess CHCHD1 expression. Correlations with clinical features were analyzed using Pearson coefficients. Prognostic relevance was evaluated using receiver operating characteristic analysis. Functional studies in SMMC-7721 cells included transwell migration/invasion assays, as well as western blotting, to assess epithelial-mesenchymal transition (EMT) markers and transforming growth factor (TGF)-β1 signaling. Gene set enrichment analysis (GSEA), single-cell RNA sequencing (scRNA-seq), and immune infiltration analyses were conducted to investigate immunoregulatory functions. CHCHD1 expression was significantly upregulated in HCC tissues (1.38-fold, < 0.001) and correlated positively with tumor size ( = 0.45), vascular invasion ( = 0.56), and advanced Barcelona Clinic Liver Cancer stage ( = 0.62; all < 0.001). High CHCHD1 predicted shorter progression-free survival (area under the curve = 0.938; 95% confidence interval 0.910-0.965; = 0.039). Overexpression of CHCHD1 enhanced cell migration and invasion, promoted EMT (downregulation of E-cadherin and upregulation of vimentin), and activated TGF-β1 signaling. GSEA linked CHCHD1 to immune-related pathways. scRNA-seq localized CHCHD1 to myeloid-derived suppressor cells, showing potential interactions with TGF-β receptor 1. CHCHD1 expression correlated with Th2 cell infiltration ( = 0.57, = 0.025) and programmed cell death 1 expression ( = 0.027). CHCHD1 promotes EMT and immune evasion in HCC via TGF-β1 signaling, implicating it as a promising biomarker and therapeutic target. - Source: PubMed
Publication date: 2025/09/29
Chenzhou XuFei Shen - To identify circadian clock (CC)-related key genes with clinical significance, providing potential biomarkers and novel insights into the CC of ovarian cancer (OC). Based on the RNA-seq profiles of OC patients in The Cancer Genome Atlas (TCGA), we explored the dysregulation and prognostic power of 12 reported CC-related genes (CCGs), which were used to generate a circadian clock index (CCI). Weighted gene co-expression network analysis (WGCNA) and protein-protein interaction (PPI) network were used to identify potential hub genes. Downstream analyses including differential and survival validations were comprehensively investigated. Most CCGs are abnormally expressed and significantly associated with the overall survival (OS) of OC. OC patients with a high CCI had lower OS rates. While CCI was positively related to core CCGs such as , it also showed significant associations with immune biomarkers including CD8 T cell infiltration, the expression of and , and the expression of interleukins (, , and ) and steroid hormones-related genes. WGCNA screened the green gene module to be mostly correlated with CCI and CCI group, which was utilized to construct a PPI network to pick out 15 hub genes (, , , , , , , , , , , , , NDUFC1, ) related to CC. Most of them can exert prognostic values for OS of OC, and all of them were significantly associated with immune cell infiltration. Additionally, upstream regulators including transcription factors and miRNAs of key genes were predicted. Collectively, 15 crucial CC genes showing indicative values for prognosis and immune microenvironment of OC were comprehensively identified. These findings provided insight into the further exploration of the molecular mechanisms of OC. - Source: PubMed
Publication date: 2023/06/20
Zhao LianfangTang YuqinYang JiayanLin FangLiu XiaofangZhang YongqiangChen Jianhui - Yes-associated protein 1 (YAP1) is the main downstream effector of the Hippo signaling pathway, which is involved in tumorigenesis. This study aimed to comprehensively understand the prognostic performances of YAP1 expression and its potential mechanism in pan-cancers by mining databases. The YAP1 expression was evaluated by the Oncomine database and GEPIA tool. The clinical significance of YAP1 expression was analyzed by the UALCAN, GEPIA, and DriverDBv3 database. Then, the co-expressed genes with YAP1 were screened by the LinkedOmics, and annotated by the Metascape and DAVID database. Additionally, by the MitoMiner 4.0 v tool, the YAP1 co-expressed genes were screened to obtain the YAP1-associated mitochondrial genes that were further enriched by DAVID and analyzed by MCODE for the hub genes. YAP1 was differentially expressed in human cancers. Higher YAP1 expression was significantly associated with poorer overall survival and disease-free survival in adrenocortical carcinoma (ACC), brain Lower Grade Glioma (LGG), and pancreatic adenocarcinoma (PAAD). The LinkedOmics analysis revealed 923 co-expressed genes with YAP1 in adrenocortical carcinoma, LGG and PAAD. The 923 genes mainly participated in mitochondrial functions including mitochondrial gene expression and mitochondrial respiratory chain complex I assembly. Of the 923 genes, 112 mitochondrial genes were identified by MitoMiner 4.0 v and significantly enriched in oxidative phosphorylation. The MCODE analysis identified three hub genes including CHCHD1, IDH3G and NDUFAF5. Our findings showed that the YAP1 overexpression could be a biomarker for poor prognosis in ACC, LGG and PAAD. Specifically, the YAP1 co-expression genes were mainly involved in the regulation of mitochondrial function especially in oxidative phosphorylation. Thus, our findings provided evidence of the carcinogenesis of YAP1 in human cancers and new insights into the mechanisms underlying the role of YAP1 in mitochondrial dysregulation. - Source: PubMed
Publication date: 2021/06/11
Wu BaojinTang XinjieKe HonglinZhou QiongZhou ZhaopingTang ShaoKe Ronghu - Several genetic loci have been reported to be significantly associated with coronary artery disease (CAD) by multiple genome-wide association studies (GWAS). Nevertheless, the biological and functional effects of these genetic variants on CAD remain largely equivocal. In the current study, we performed an integrative genomics analysis by integrating large-scale GWAS data (N = 459,534) and 2 independent expression quantitative trait loci (eQTL) datasets (N = 1890) to determine whether CAD-associated risk single nucleotide polymorphisms (SNPs) exert regulatory effects on gene expression. By using Sherlock Bayesian, MAGMA gene-based, multidimensional scaling (MDS), functional enrichment, and in silico permutation analyses for independent technical and biological replications, we highlighted 4 susceptible genes (CHCHD1, TUBG1, LY6G6C, and MRPS17) associated with CAD risk. Based on the protein-protein interaction (PPI) network analysis, these 4 genes were found to interact with each other. We detected a remarkably altered co-expression pattern among these 4 genes between CAD patients and controls. In addition, 3 genes of CHCHD1 (P = .0013), TUBG1 (P = .004), and LY6G6C (P = .038) showed significantly different expressions between CAD patients and controls. Together, we provide evidence to support that these identified genes such as CHCHD1 and TUBG1 are indicative factors of CAD. - Source: PubMed
Zhong YigangChen LiuyingLi JingjingYao YinghaoLiu QiangNiu KaimengMa YunlongXu Yizhou