| http://purl.uniprot.org/citations/35866661 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/35866661 | http://www.w3.org/2000/01/rdf-schema#comment | "HnRNP K is a heterogeneous nuclear ribonucleoprotein and has been identified as an oncogene in most solid tumors via regulating gene expression or alternative splicing of genes by binding both DNA and pre-mRNA. However, how hnRNP K affects tumorigenesis and regulates the gene expression in cervical cancer (CESC) remains to be elucidated. In these data, higher expression of hnRNP K was observed in CESC and was negatively correlated with the patient survival time. We then overexpressed hnRNP K (hnRNP K-OE) and found that its overexpression promoted cell proliferation in HeLa cells (P = 0.0052). Next, global transcriptome sequencing (RNA-seq) experiments were conducted to explore gene expression and alternative splicing profiles regulated by hnRNP K. It is shown that upregulated genes by hnRNP K-OE were associated with inflammatory response and an apoptotic process of neuron cells, which involves in cancer. In addition, the alternative splicing of those genes regulated by hnRNP K-OE was associated with transcriptional regulation. Analysis of the binding features of dysregulated transcription factors (TFs) in the promoter region of the inflammatory response genes regulated by hnRNP K revealed that hnRNP K may modulate the expression level of genes related to inflammatory response by influencing the alternative splicing of TFs. Among these hnRNP K-TFs-inflammatory gene regulatory networks, quantitative reverse transcription polymerase chain reaction (RT-qPCR) experiments and gene silencing were conducted to verify the hnRNP K-IRF1-CCL5 axis. In conclusion, the hnRNP K-TFs-inflammatory gene regulatory axis provides a novel molecular mechanism for hnRNP K in promoting CESC and offers a new therapeutic target."xsd:string |
| http://purl.uniprot.org/citations/35866661 | http://purl.org/dc/terms/identifier | "doi:10.1177/15353702221110649"xsd:string |
| http://purl.uniprot.org/citations/35866661 | http://purl.uniprot.org/core/author | "Chen D."xsd:string |
| http://purl.uniprot.org/citations/35866661 | http://purl.uniprot.org/core/author | "Liu S."xsd:string |
| http://purl.uniprot.org/citations/35866661 | http://purl.uniprot.org/core/author | "Tan J."xsd:string |
| http://purl.uniprot.org/citations/35866661 | http://purl.uniprot.org/core/author | "Duan Y."xsd:string |
| http://purl.uniprot.org/citations/35866661 | http://purl.uniprot.org/core/author | "You R."xsd:string |
| http://purl.uniprot.org/citations/35866661 | http://purl.uniprot.org/core/date | "2023"xsd:gYear |
| http://purl.uniprot.org/citations/35866661 | http://purl.uniprot.org/core/name | "Exp Biol Med (Maywood)"xsd:string |
| http://purl.uniprot.org/citations/35866661 | http://purl.uniprot.org/core/pages | "1479-1491"xsd:string |
| http://purl.uniprot.org/citations/35866661 | http://purl.uniprot.org/core/title | "HnRNP K regulates inflammatory gene expression by mediating splicing pattern of transcriptional factors."xsd:string |
| http://purl.uniprot.org/citations/35866661 | http://purl.uniprot.org/core/volume | "248"xsd:string |
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