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A novel prognostic risk model for cervical cancer based on immune checkpoint HLA-G-driven differentially expressed genes [HeLa]

ABSTRACT: A novel prognostic risk model for cervical cancer based on immune checkpoint HLA-G-driven differentially expressed genes [HeLa]

PROVIDER: PRJNA858423 | ENA |

REPOSITORIES: ENA

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A novel prognostic risk model for cervical cancer based on immune checkpoint HLA-G-driven differentially expressed genes [HeLa]

Project description:The aim of this study was to construct and validate a prognostic risk model to predict the overall survival (OS) of patients with cervical cancer, providing a reference for individualized clinical treatment that may lead to better clinical outcomes. HLA-G-driven DEG signature consisting of the eight most important prognostic genes CD46, LGALS9, PGM1, SPRY4, CACNB3, PLIN2, MSMO1, and DAGLB was identified as a key predictor of cervical cancer. To summarize, we developed and validated a novel prognostic risk model for cervical cancer based on HLA-G-driven DEGs, and the prognostic signature showed great ability in predicting the overall survival of patients with cervical cancer.

2022-07-19 | GSE208117 | GEO

A novel prognostic risk model for cervical cancer based on immune checkpoint HLA-G-driven differentially expressed genes [SiHa]

2022-07-19 | GSE208118 | GEO

A novel prognostic risk model for cervical cancer based on immune checkpoint HLA-G-driven differentially expressed genes

Project description:A novel prognostic risk model for cervical cancer based on immune checkpoint HLA-G-driven differentially expressed genes

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A novel prognostic risk model for cervical cancer based on immune checkpoint HLA-G-driven differentially expressed genes [SiHa]

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High expression of SerpinA1 and SerpinA3 in HLA-positive cervical cell carcinomas

Project description:In cervical cancer, an important mechanism by which tumour cells escape immune surveillance is loss of HLA class I, enabling tumours to evade recognition and lysis by cytotoxic T lymphocytes. Some tumours, however, escape from immune surveillance without accumulating defects in antigen presentation. We hypothesized that tumours with no or partial loss of HLA class I develop alternative mechanisms to prevent immune surveillance. To investigate this hypothesis, genome-wide expression profiling using Illumina arrays was performed on cervical squamous cell carcinomas showing overall loss of HLA class I, partial and normal HLA class I protein expression. Statistical analyses revealed no significant differences in gene expression between tumours with partial (n = 11) and normal HLA class I expression (n = 10). Comparison of tumours with normal/partial HLA class I expression (n = 21) with those with overall loss of HLA class I expression (n = 11) identified 150 differentially expressed genes. Most of these genes were involved in the defense response (n = 27), and, in particular, inflammatory and acute phase responses. Especially SerpinA1 and SerpinA3 were found to be upregulated in HLA positive tumours (3.6 and 8.2 fold, respectively), and this was confirmed by real-time PCR and immunohistochemistry. In a group of 117 tumours, high SerpinA1 and SerpinA3 expression in association with normal/partial HLA expression correlated significantly with poor overall survival (p = 0.035 and p = 0.05, respectively). This study shows that HLA positive tumours are characterized by a higher expression of genes associated with an inflammatory profile and that expression of the acute phase proteins SerpinA1 and SerpinA3 in HLA positive tumours is associated with worse prognosis. Keywords: Cell type comparison

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Genome-wide analysis of gene expression regulated by FSCN1 in cervical cancer HeLa cells

Project description:FSCN1 has been reported to be dysregulated in cervical cancers. However, the genome-wide regulated targets of FSCN1 is still unclear in cervical cancers. Here, the gene expression profile of HeLa cells transfected with FSCN1 shRNA (shFSCN1) were compared with cells transfected with empty vector (shCtrl). The results showed that shFSCN1 extensively affects the transcriptional level of 5, 043 genes in HeLa cells. There were more up-regulated genes (3, 870) than down-regulated ones (1, 173) after FSCN1 was knocked down in HeLa cells. GO analysis showed that the up-regulated genes were associated with transcription regulation and DNA binding. The down-regulated genes were enriched in some cancer associated pathway including angiogenesis and cell adhesion. In particular, FSCN1 positilvely regulated ANGPTL4 in HeLa cells. Compared to normal tissue, both FSCN1 and ANGPTL4 showed a higher expression in cervical tumor tissue. Moreover, ANGPTL4 was also positilvely correlated with expression of FSCN1 in cervical tumor tissue of TCGA. In conclusion, our study provide important cues for further study on the regulatory mechanism of FSCN1 in cervical cancer.

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exosomal microRNA maps of HeLa cell exosome vs human cervical epithelial cell exosome [miRNA-seq]

Project description:We aimed to compare the exosomal microRNA profile form HeLa cell line with that from human cervical epithelial cell(Hcer)line.exosomes were isolated from conditioned medium of HeLa cell and HCer cell,3 samples for each group.Exosomal microRNAs were sequenced on Proton Sequencers according to Ion PI Hi-Q Sequencing 200 Kit (Life Technologies).According to the results of miRNA sequencing, we found a total 371 different miRNAs the amount of which reach to 10 fold differece between two groups.

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2017-09-06 | GSE103475 | GEO

RNA-seq analysis of HeLa cells overexpressing histone methyltransferase KMT2B

Project description:KMT2B，a major H3K4 tri-methyltransferase, contributes to the development of various cancers. However, its role in cervical cancer is unclear. We found that KMT2B is upregulated in cervical cancer tissues, which is significantly associated with poor prognosis.To investigate the underlying mechanism of KMT2B in the progression of cervical cancer, we established stable KMT2B-overexpression HeLa cells.Then we compared the whole genome mRNA expression profile of KMT2B overexpression and control HeLa cells using RNA-seq.

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