C6orf120
- Known as:
- C6orf120
- Catalog number:
- 003179A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- C6orf120
Related genes to: C6orf120
- Gene:
- C6orf120 NIH gene
- Name:
- chromosome 6 open reading frame 120
- Previous symbol:
- -
- Synonyms:
- bA160E12.4
- Chromosome:
- 6q27
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-01
- Date modifiied:
- 2016-09-30
Related products to: C6orf120
Related articles to: C6orf120
- C6ORF120 is an N-glycosylated secretory protein with unknown functions, particularly in the context of inflammatory bowel disease (IBD). This study aimed to clarify the role of C6ORF120 in IBD and delineate the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/04/06
Zhang JianQiao RuiLi Xin - Background Emerging evidence indicates that C6ORF120 is highly expressed in the liver and may modulate immune responses in various hepatic disorders. However, its role in hepatic lipid metabolism and metabolic dysfunction-associated steatotic liver disease (MASLD) is unexplored. This study aimed to elucidate the effects and potential mechanisms of C6ORF120 on hepatic lipogenesis. Methods C6ORF120 expression in MASLD was assessed using patient serum and the Gene Expression Omnibus (GEO) database. A high-fat diet-induced MASLD model was established in C6orf120-KO rats. Fatty acid-induced lipid accumulation models were generated in primary hepatocytes, HepG2 and Huh7 cells. These models were employed to investigate the effects of C6ORF120 on hepatic lipogenesis and MASLD progression. Results C6ORF120 expression was significantly upregulated in MASLD patients and obese rat models. Genetic deletion of C6ORF120 markedly alleviated high-fat diet-induced steatosis in the liver of rats. In vitro, C6orf120 gene deficiency attenuated lipid accumulation and suppressed key lipogenic genes (such as fatty acid synthase (Fasn), phospho-acetyl coenzyme carboxylase (p-ACC), sterol regulatory element binding protein-1c (Srebp1c)) in primary hepatocytes and HepG2 cells. Conversely, C6ORF120 overexpression increased lipid accumulation in HepG2 cells. RNA sequencing analysis showed that lipid metabolism pathway and peroxisome proliferators activated receptor (PPAR) signaling pathway were significantly altered in the liver of C6orf120-KO rats. We demonstrated that C6ORF120 may regulate lipid metabolism through the hepatic PPARα, which is involved in fatty acid production and lipid oxidation. Further, we found that serum C6ORF120 expression was correlated with clinical indicators in patients with MASLD. Conclusion This study preliminarily revealed a novel function for C6ORF120 in hepatic lipid metabolism via affecting the PPAR pathway. The result identifies C6ORF120 as a novel regulator of hepatic lipid metabolism through PPARα-dependent mechanisms, offering potential therapeutic targets for MASLD. - Source: PubMed
Publication date: 2025/10/24
Wang PengZhang JianWang XinLiu HuiYi YunyunLiu YaliZhang JingLi Xin - The mC RNA modifications have been implicated in the pathogenesis of urothelial carcinoma and hold potential as prognostic biomarkers for muscle-invasive bladder cancer (MIBC) patients. In this study, we developed an MIBC-risk model by integrating mC modification-related genes and differentially expressed genes using Nanopore sequencing and a machine learning approach. Compared to our previous research, we observed that mC modifications are more functional, with the most enriched regions being the 3'UTR and exons. Our analysis revealed differential mC methylation sites in several well-characterized cancer-related genes, including BMI1, PTEN, MALAT1, FADD, STAT5A, BIRC6, FOXO3, CCNG1, PAK2, UBE2L3, SMARCB1, and TUG1. Functional enrichment analysis demonstrated significant involvement of these genes in key oncogenic pathways, particularly DNA damage response, double-strand break repair, p53 signaling, MAPK cascade, NF-κB signaling, and cell proliferation/migration pathways. Unlike models based on single factors, the combination of mC modification-related genes and differentially expressed genes resulted in a more effective classification model. This approach yielded an optimized 11-gene prognostic signature comprising GGA1, NUMBL, ECHDC2, NLRC5, EIF2D, GJA1, XPC, DAZAP2, C6orf120, WDR45, and CES1, which demonstrated superior predictive performance in TCGA MIBC patients. These findings establish mC RNA modification patterns as promising molecular signatures for MIBC prognosis and potential therapeutic targets. - Source: PubMed
Publication date: 2025/09/25
Zhang LiliZhou LiyingXu WenruiWu PengjieChen WenLi HexinSun GaoyuanXu SiyuanTang XiaokunLiu LipinZhang YaqunZhong Qiuzi - The vascular endothelium plays a pivotal role in modulating various physiological processes and its dysfunction is fundamental to the development of numerous vascular and non‑vascular diseases. Chromosome 6 open reading frame 120 (C6ORF120) has been implicated in cellular processes such as apoptosis, inflammation, immunomodulation and fibrosis. However, the specific effects of C6ORF120 on endothelial cell function remain unclear. The present study aimed to explore the potential role of C6ORF120 in endothelial dysfunction and its underlying molecular mechanisms. It synthesized recombinant C6ORF120 protein (rC6ORF120) and assessed its effects on human umbilical vein endothelial cells (HUVECs) through various functional assays, including the CCK‑8 assay for proliferation, scratch assay for migration and tube formation assay for angiogenesis. Additionally, immunofluorescence (IF) and western blotting (WB) were employed to evaluate endothelial‑mesenchymal transition (EndMT). The present study also quantified the expression of key proteins within the PI3K/Akt signaling pathway to elucidate its role in mediating the effects of rC6ORF120 on HUVECs. Treatment with rC6ORF120 significantly enhanced HUVEC proliferation (200 ng/ml vs. control at 72 h, 1.14±0.01 vs. 1.05±0.02; t=8.15; P<0.001) and induced phenotypic changes. In migration and angiogenesis assays, rC6ORF120‑treated HUVECs exhibited increased wound closure (37.69±2.74% vs. 66.16±6.13%; t=7.35; P=0.002) and angiogenesis assays showed significant improvements in tube formation parameters such as total tubule length (77,199.67±4,684.88 µm vs. 96,203.00±3,354.89 µm; t=5.71; P=0.002). WB and IF analyses both indicated that rC6ORF120 promotes EndMT in HUVECs. Furthermore, rC6ORF120 treatment increased PI3K/Akt phosphorylation significantly compared with controls (p‑PI3K; 1.57±0.18 vs. 1.00±0.00; t=5.64; P=0.005). LY294002 significantly reversed these effects on EndMT and angiogenesis (P<0.05), while the effect on cell migration was less pronounced (P=0.565). Our study highlights the critical role of C6ORF120 in HUVECs, promoting proliferation, migration, angiogenesis and EndMT, which are mediated, at least in part, by the PI3K/Akt pathway. - Source: PubMed
Publication date: 2025/06/20
Lin YingyingWang XinLi YanyanCui XinyuZhu NaLi Xin - Vitamin A (VA) and its active form, retinoic acid (RA), are crucial for preserving hepatic stellate cells (HSCs) quiescence and reversing fibrosis. While C6orf120 is known to be involved in HSC activation, its role in RA signaling is unclear. This study found that C6orf120 knockdown markedly reduced CCL4-induced liver fibrosis and TGF-β1-induced activation in LX-2 cells, a human HSC line. This inhibition was associated with enhanced RA signaling, particularly affecting the RA receptor beta (RARβ). Inhibition of RARβ significantly reversed the protective effects of C6orf120 knockdown, indicating that RARβ signaling contributes to the inhibitory effect of C6orf120 knockdown on HSC activation. Our results reveal that C6orf120 inhibition could be a therapeutic strategy for liver fibrosis by regulating RARβ signaling. - Source: PubMed
Publication date: 2025/02/04
Lin YingyingWang XinCui XinyuZhu NaLi YanyanLi Xin