Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1045304 | ENA |
REPOSITORIES: ENA
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Project description:MicroRNAs (miRNAs or miRs) play essential roles in the initiation and progression of human tumors, including cervical cancer. However, the mechanisms underlying their actions in cervical cancer remain unclear. The present study aimed to evaluate the functional role of miR‑130a‑3p in cervical cancer. Cervical cancer cells were transfected with a miRNA inhibitor (anti‑miR‑130a‑3p) and a negative control. Adhesion‑independent cell proliferation, migration and invasion were evaluated. The findings presented herein demonstrated that miR‑130a‑3p was overexpressed in HeLa, SiHa, CaSki, C‑4I and HCB‑514 cervical cancer cells. The inhibition of miR‑130a‑3p significantly reduced the proliferation, migration and invasion of cervical cancer cells. The canonical delta‑like Notch1 ligand (DLL1) was identified as a possible direct target of miR‑103a‑3p. The DLL1 gene was further found to be significantly downregulated in cervical cancer tissues. On the whole, the present study demonstrates that miR‑130a‑3p contributes to the proliferation, migration and invasion of cervical cancer cells. Therefore, miR‑130a‑3p may be used as a biomarker to determine cervical cancer progression.
2023-03-10 | GSE224301 | GEO
Project description:Gene expression of leaders and laggers MiaPaCa-2 pancreatic cancer cells during perineural invasion
| PRJNA854683 | ENA
Project description:To investigate the mechanisms of cancer cell migration during perineural invasion in pancreatic cancer, we injected fluorescently labelled MiaPaCA-2 cells in the sciatic nerves and collected the leader and lagger cells.
2023-03-31 | GSE207319 | GEO
Project description:Gigaxonin, the GAN gene product, is a E3 ubiquitin ligase adaptor and is involved in neural cell and fibroblast intermediate filament processing. We have previously shown that gigaxonin in association with p16 ubiquitinates NF-κB in head and neck cancer. The cancer genomic database search has shown higher frequency of GAN gene exon 8 single nucleotide polymorphism (SNP, rs2608555), c.1293 C>T, p.Y431Y, in the normal Caucasian population (44.25% vs <20% in other populations). To determine whether this SNP is related to tumor development, we analyzed normal and tumor DNAs of cervical and head and neck cancer subjects and have found higher frequency of the SNP (Tumor 47% vs 25% normal, p=0.0017) in tumor samples. Although there was no relationship to HPV status, an inverse relationship to tumor recurrence and metastasis was observed. Two cervical cancer cell lines, ME180 and HT3, containing the SNP (T/T alleles) showed higher gigaxonin expression, reduced in vitro tumor cell growth and enhanced cisplatin sensitivity in comparison to 5 other cervical and 5 head and neck cancer cell lines containing the C allele (C/C or C/T alleles). CRISPR-Cas9 mediated conversion of T/T to C/C alleles of the ME180 cell line led to decreased gigaxonin expression, enhanced expression of snail, and twist (Epithelial to Mesenchymal transition - EMT markers) and increased in vitro tumor cell growth including invasion through Matrigel. Re-expression of gigaxonin in CRISPR-Cas9 cells using a lentiviral system resulted in increased expression of gigaxonin and reduced expression of snail accompanied by decreased in vitro cell growth. Mouse tail vein injection studies showed lung metastasis of CRISP-Cas9 cells which was inhibited in gigaxonin overexpressing cells. Our results strongly suggest that GAN gene exon 8 SNP correlates with gigaxonin expression, and inhibition of EMT phenotype in human tumors.
2024-03-13 | GSE179424 | GEO
Project description:Background and Purpose: Our previous work reported that galaxamide, a cyclopeptide extracted from the seaweed Galaxaura filamentosa, showed antiproliferative activity against HeLa cells by MTT assay. However, the therapeutic effects in vivo and potential mechanisms to eliminate cervical cancer cells remain unknown. Experimental Approach: HeLa cells were obtained as a cervical carcinoma in vitro model. The growth-inhibitory effects of galaxamide in HeLa cells and xenograft mouse models were investigated. RNA-seq was employed to analyse the main target of galaxamide in HeLa cells. Immunostaining, qRT‒PCR and Western blotting were applied to test the pharmacological effects in vitro and in vivo. Key Results: Galaxamide significantly inhibited cell growth, colony formation, migration, and invasion and induced cell apoptosis by inhibiting the Wnt signalling pathway in HeLa cells. RNA sequencing revealed that galaxamide regulated stemness via the Wnt6 signalling pathway in HeLa cells. By analysing The Cancer Genome Atlas database (TCGA), Wnt6 was found to be negatively/positively correlated with stemness- and apoptosis-related genes in human cervical cancer. Cancer stem-like cells (CSCs) isolated and enriched from HeLa cells demonstrated elevated Wnt6 and β-catenin genes compared with nonstem HeLa cells. After galaxamide treatment, CSCs showed abrogation of sphere-forming ability, along with inhibition of stemness-related and Wnt pathway genes. Galaxamide treatment was accompanied by the induction of apoptosis in HeLa cells, which was consistent with the results in BALB/c nude mice. Conclusion and Implications: Our results provide preclinical evidence that suppression of stemness by downregulating the Wnt signalling pathway is the molecular mechanism by which galaxamide effectively inhibits cell growth and induces apoptosis in cervical cancer cells.
2023-04-03 | GSE228509 | GEO
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.
2022-01-20 | GSE149450 | GEO
Project description:Using chromatin immunoprecipitation and high-resolution tiling arrays covering the human genome, we render a genome-wide map of p73 DNA binding sites in ME180 human cervical carcinoma cells.
2010-09-10 | GSE18650 | GEO
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.
2022-08-03 | GSE209928 | GEO
Project description:Perineural invasion (PNI) is a pivotal prognostic factor in pancreatic cancer, associated with aggressive tumor behavior and adverse patient outcomes. Despite its recognized clinical impact, the molecular mechanisms underlying PNI are not well understood. In this study, we isolated perineural invasion-associated cancer-associated fibroblasts (pCAFs), which demonstrated a markedly enhanced capacity to promote neural invasion in pancreatic cancer compared to non-perineural invasion-associated CAFs (npCAFs). Utilizing single-cell, high-throughput sequencing, and metabolomics, we identified a significant upregulation of glycolysis in pCAFs, fostering a high-lactate tumor microenvironment conducive to cancer progression. pCAFs-derived lactate is absorbed by tumor cells, facilitating histone H3K18 lactylation. This epigenetic modification activates the transcription of neural invasion-associated genes such as L1CAM and SLIT1, thereby driving PNI in pancreatic cancer. Further exploration of metabolic reprogramming in pCAFs revealed enhanced acetylation of the glycolytic enzyme GAPDH, correlated with increased enzymatic activity and glycolytic flux. Targeting of GAPDH and lactylation modifications significantly inhibits neural invasion in a KPC mouse model. Clinical data suggested that high levels of H3K18 lactylation correlate with severe PNI and poorer patient prognosis. Our findings provide critical insights into the role of pCAFs in the PNI of pancreatic cancer, highlighting glycolytic reprogramming and lactate-driven histone modifications as potential therapeutic targets for PDAC.
2025-03-19 | GSE290654 | GEO
Project description:Perineural invasion (PNI) is a pivotal prognostic factor in pancreatic cancer, associated with aggressive tumor behavior and adverse patient outcomes. Despite its recognized clinical impact, the molecular mechanisms underlying PNI are not well understood. In this study, we isolated perineural invasion-associated cancer-associated fibroblasts (pCAFs), which demonstrated a markedly enhanced capacity to promote neural invasion in pancreatic cancer compared to non-perineural invasion-associated CAFs (npCAFs). Utilizing single-cell, high-throughput sequencing, and metabolomics, we identified a significant upregulation of glycolysis in pCAFs, fostering a high-lactate tumor microenvironment conducive to cancer progression. pCAFs-derived lactate is absorbed by tumor cells, facilitating histone H3K18 lactylation. This epigenetic modification activates the transcription of neural invasion-associated genes such as L1CAM and SLIT1, thereby driving PNI in pancreatic cancer. Further exploration of metabolic reprogramming in pCAFs revealed enhanced acetylation of the glycolytic enzyme GAPDH, correlated with increased enzymatic activity and glycolytic flux. Targeting of GAPDH and lactylation modifications significantly inhibits neural invasion in a KPC mouse model. Clinical data suggested that high levels of H3K18 lactylation correlate with severe PNI and poorer patient prognosis. Our findings provide critical insights into the role of pCAFs in the PNI of pancreatic cancer, highlighting glycolytic reprogramming and lactate-driven histone modifications as potential therapeutic targets for PDAC.
2025-03-05 | GSE290845 | GEO