Ask about this productRelated genes to: CPSF4 Blocking Peptide
- Gene:
- CPSF4 NIH gene
- Name:
- cleavage and polyadenylation specific factor 4
- Previous symbol:
- -
- Synonyms:
- NAR, CPSF30
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-31
- Date modifiied:
- 2016-10-05
Related products to: CPSF4 Blocking Peptide
Related articles to: CPSF4 Blocking Peptide
- Hepatocellular carcinoma (HCC) remains a global health challenge with a high recurrence rate, highlighting the need to decipher its underlying molecular mechanisms. While circular RNAs (circRNAs) are known to regulate gene expression, the landscape of competitive splicing-the dynamic balance between back-splicing and linear splicing-during HCC initiation and recurrence remains largely unexplored. Leveraging rRNA-zero RNA-seq data from GSE169289 (comprising 34 primary, recurrent, and non-recurrent HCC samples with paired controls), this study utilized an upgraded SUVA pipeline to systematically profile circRNA-associated alternative splicing events. By integrating four distinct algorithms, we identified 9,652 high-confidence circRNAs. Our analysis revealed extensive differential splicing events distinguishing tumor from normal tissues, and notably, recurrent from non-recurrent tumors, with host genes enriched in chromatin remodeling and ubiquitin-dependent pathways. Specifically, we observed a conserved attenuation in the competitive splicing of the LARP1B circRNA in tumor tissues, which correlated with host gene downregulation and poor prognosis. In the context of recurrence, circ-KLHL8 exhibited specific splicing suppression; in silico modeling suggests a potential mechanism where circ-KLHL8 loss relieves the sponging of miRNAs, thereby suppressing the tumor suppressor GLYCTK. Furthermore, RBP-circRNA co-regulatory network analysis implicated HNRNPU and CPSF4 as potential upstream regulators of initiation-related splicing, and DKC1 as a modulator of recurrence-associated events. Collectively, this study provides the first systematic characterization of the competitive splicing landscape in HCC, proposing a novel theoretical framework and candidate targets for diagnostic and therapeutic interrogation. - Source: PubMed
Publication date: 2026/05/14
Jiang SunluCui NingNie LeiShen JianZhu XianminLi Hong - Hepatocellular carcinoma (HCC), which predominantly manifests as a malignant form of primary liver cancer, remains resistant to existing therapies in many patients. Therefore, elucidating the cellular processes and signaling networks driving HCC progression and discovering novel treatment targets remain key areas of research. , , and are closely associated with liver cancer, but the relationship between them is unclear. , , and levels were quantified using RT-qPCR. expression was analyzed through Western blotting. Liver tumor cell viability was assessed using CCK8 assays. The metastatic potential of cells was primarily evaluated using wound healing and Transwell assays. 's impact on tumors was validated through live animal experiments by inducing subcutaneous tumor formation in nude mice. RNAhybrid and TargetScan analyzed potential target regions in and . Our study demonstrates that reducing expression can inhibit hepatoma cell proliferation, migration, and invasive abilities. Specifically, knocking down can reduce the expression of . Knocking down can suppress liver cancer development in live animal models. In addition, can bind and and down-regulate the expression of . In summary, promotes the proliferation, migration, and invasion of HCC cells by inhibiting / axis. - Source: PubMed
Publication date: 2025/11/24
Ge PengXinNiu SensenFang MinXu QianruZhang WeiXu JiliangYang FengWang YangkuiShi TianluLiu Hongjin - Lung cancer is the most common cancer worldwide, and approximately 30% of lung cancer patients will develop brain metastases. Serine/threonine kinase 39 (STK39) plays a significant role in various malignancies. However, the role and mechanism of STK39 in lung cancer brain metastasis have not been reported. - Source: PubMed
Publication date: 2025/05/21
Shu YueDong YunzhuLi BoWang YutongLiao QuanyangSu ZiqinWang JunZuo PinYuan HongpinWang ChunLi ShujuanFan YaodongSu Xiaosan - Hepatocellular carcinoma (HCC), a prevalent and highly malignant form of liver cancer, poses significant global health challenges. Previous studies have suggested that alterations in cleavage and polyadenylation specificity factors (CPSFs) play a role in the development and prognosis of HCC. Despite these insights, a thorough evaluation of CPSFs' expression levels, prognostic value and association with immune infiltration in HCC is lacking. To address this gap, the present study conducted a systematic analysis leveraging multiple bioinformatics databases to elucidate the functions of CPSFs in HCC. To comprehensively investigate the role of CPSFs in HCC, a diverse array of bioinformatics tools and publicly accessible datasets were utilized. The present study investigated the gene expression patterns, clinicopathological correlations, and diagnostic and prognostic capabilities of CPSFs. Furthermore, genetic variations, co-expression networks and the role of CPSFs in immune cell infiltration and tumor-related pathways were examined. To elucidate the biological functions of CPSF-associated genes, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were integrated. For experimental validation, reverse transcription-quantitative polymerase chain reaction was used to assess gene expression and the Cell Counting Kit-8 assay was utilized to evaluate the effects of CPSFs on HCC cell proliferation. Our analysis offers valuable insights into the molecular mechanisms through which CPSFs contribute to HCC progression. The current findings suggest that CPSFs, particularly CPSF1, CPSF3, CPSF4 and CPSF6, exhibit significant transcriptional upregulation in HCC, with their overexpression closely tied to advanced tumor progression. These CPSFs showed diagnostic and prognostic significance in HCC. Additionally, CPSF expression was associated with immune cell infiltration and activation status. Functional enrichment analysis indicated that CPSF1, CPSF3, CPSF4, CPSF6 and CPSF7 are involved in cancer-related signaling pathways, highlighting their role in tumor immune modulation. Experimental validation demonstrated that the expression of CPSF3 and CPSF7 was notably greater in the HCC cell lines than in the normal liver cells. Knockdown of CPSF3 and CPSF7 inhibited HCC cell proliferation, suggesting their potential oncogenic roles. This research offers an in-depth evaluation of the expression patterns, prognostic relevance and immune modulation-related functions of CPSFs in HCC. The observed upregulation of CPSFs in HCC, coupled with their association with poor clinical outcomes and immune system activation, highlights their potential as prognostic indicators. Nonetheless, additional experimental studies are needed to fully elucidate the molecular mechanisms and clinical significance of CPSFs in HCC. - Source: PubMed
Publication date: 2025/04/28
Lu YuxiangWang TingYan XiuliZhang Hui - Drug-resistant influenza demands novel antiviral treatments. Non-structural protein 1 (NS1) of influenza A virus (IAV) regulates the viral life cycle and host immune response, thus becoming a promising therapeutic target. The atractylenolide (ACT) -Ⅲ exhibits notable anti-IAV efficacy; however, its in vivo anti-IAV activity and the underlying mechanisms need further exploration. - Source: PubMed
Publication date: 2025/03/29
Liang JinlongGuo HuiyiYang YanLiang GuorunChen ZhixuanLi DanLiang HaoQiu JiayinMei QinghuaLiu ShuwenYang JieWu Wenjiao