Genome-wide analysis of gene expression to identify the probably functionally relevant pathways in cervical cancer progression
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE67522 | GEO | 2015/04/02
SECONDARY ACCESSION(S): PRJNA280126
REPOSITORIES: GEO
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Project description:Identification of genes and pathways relevant to Cervical cancer pathogenesis. The study also aimed at identifying probable mechanistic differences in the low and high HOTAIR expressing cervical cancers patients . Total RNA obtained from HPV negative histologically normal controls, HPV16 positive non-malignants and HPV16 positive cervical cancers having either low or high HOTAIR expression levels were compared to identify transcriptome level differences.
2015-04-02 | E-GEOD-67522 | biostudies-arrayexpress
Project description:The long-non-coding HOX transcript antisense intergenic RNA (HOTAIR) was identified as significantly upregulated in breast ductal carcinoma in situ (DCIS). The aim of this study was to characterize the phenotypic effects and signaling pathways modulated by HOTAIR in early-stage breast cancer progression. We determined that HOTAIR induces premalignant phenotypic changes by increasing cell proliferation, migration, invasion and in vivo growth in normal and DCIS breast cell lines. Transcriptomic studies (RNA-seq) identified the main signaling pathways modulated by HOTAIR which include bioprocesses related to cell migration, epithelial to mesenchymal transition, extracellular matrix remodeling and activation of HIF1A, AP1 and FGFR signaling pathways among others. Similar pathways were identified as activated in primary invasive breast carcinomas with HOTAIR over-expression. We conclude that HOTAIR over-expression behaves as a positive regulator of cell growth and migration both in normal and DCIS breast cells involved with early-stage breast cancer progression.
2021-11-01 | GSE183058 | GEO
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:Affymetrix-U133-plus2.0-based gene expression analysis of laser-captured epithelium from 128 cervical tissue specimens from women enrolled in SUCCEED Cervical cancer (CC) is the second most frequent cancer in women and the third leading cause of cancer death in women worldwide. Our analysis of normal, precancerous, and cancerous cervical tissue shows that progress of the disease is a cascade of increased DNA replication/repair and cell proliferation followed by substantial metabolic shifts. The data show a sharp decrease in estrogen receptor alpha (ERα) in tumor cells, and ranking tissue specimens by estrogen-responsive gene expression correlates remarkably closely with histological pathology. Johan, den Boon, Morgridge Institute for Research at University of Wisconsin-Madison Paul, Ahlquist, Howard Hughes Medical Institute and Morgridge Institute for Research at University of Wisconsin-Madison Nicolas, Wentzensen, National Cancer Institute
2015-07-01 | GSE63514 | GEO
Project description:Affymetrix-U133-plus2.0-based gene expression analysis of laser-captured epithelium from 128 cervical tissue specimens from women enrolled in SUCCEED Cervical cancer (CC) is the second most frequent cancer in women and the third leading cause of cancer death in women worldwide. Our analysis of normal, precancerous, and cancerous cervical tissue shows that progress of the disease is a cascade of increased DNA replication/repair and cell proliferation followed by substantial metabolic shifts. The data show a sharp decrease in estrogen receptor alpha (ER?) in tumor cells, and ranking tissue specimens by estrogen-responsive gene expression correlates remarkably closely with histological pathology. Johan, den Boon, Morgridge Institute for Research at University of Wisconsin-Madison Paul, Ahlquist, Howard Hughes Medical Institute and Morgridge Institute for Research at University of Wisconsin-Madison Nicolas, Wentzensen, National Cancer Institute 24 normal, 14 CIN1 lesions, 22 CIN2 lesions, 40 CIN3 lesions, and 28 cancers specimens were cryosecrtioned and used for laser-capture, RNA extraction, two rounds of T7-mediated amplification, and cRNA biotinylation. Bio-cRNA was hybridized to Affymetrix U133-Plus2.0 arrays, scanned signals were processed through GC-RMA
2015-07-01 | E-GEOD-63514 | biostudies-arrayexpress
Project description:Comparable plasma lipid changes in patients with high-grade cervical intraepithelial neoplasia and patients with cervical cancer
2020-10-22 | MSV000086351 | GNPS
Project description:Dysregulation of glyco-gene expression in cancer can lead to aberrant glycans and glycoconjugates, which in turn can promote tumorigenesis. Cervical cancer display augmentation of aberrant sialylated glycans and increase of glyco-genes, which encoded enzymes participate in the sialylation pathways. Besides sialiltranferases, other glyco-genes, analyzed individually are reported as altered in cervical cancer. Here we show a comprehensive analysis of glyco-gene expression in cervical cancer to obtain a wide scenery of global changes in glycosylation pathways. First, we compared glyco-gene expression between normal tissue and cervical cancer. Second, we analyzed the glycogene expression in subtypes of cc to obtain hallmarks of glyco-gene expression in each case. Our results indicate that in cervical cancer the GPI-anchored biosynthesis is increased in cc while the synthesis of chondroitin and dermatan sulfate are decreased. Moreover, data show that adenocarcinoma displayed a homogenous glyco-gene expression pattern, where chondroitin /dermatan sulfate and heparan sulfate glycogenes are decreased, while keratan sulfate genes are increased. Dysregulation of glyco-gene expression in cancer can lead to aberrant glycans and glycoconjugates, which in turn can promote tumorigenesis. Cervical cancer display augmentation of aberrant sialylated glycans and increase of glyco-genes, which encoded enzymes participate in the sialylation pathways. Besides sialiltranferases, other glyco-genes, analyzed individually are reported as altered in cervical cancer. Here we show a comprehensive analysis of glyco-gene expression in cervical cancer to obtain a wide scenery of global changes in glycosylation pathways. First, we compared glyco-gene expression between normal tissue and cervical cancer. Second, we analyzed the glycogene expression in subtypes of cc to obtain hallmarks of glyco-gene expression in each case. Our results indicate that in cervical cancer the GPI-anchored biosynthesis is increased in cc while the synthesis of chondroitin and dermatan sulfate are decreased. Moreover, data show that adenocarcinoma displayed a homogenous glyco-gene expression pattern, where chondroitin /dermatan sulfate and heparan sulfate glycogenes are decreased, while keratan sulfate genes are increased.
2020-10-24 | GSE159976 | GEO
Project description:Cervical inflammasome activation and subsequent protease upregulation are potential mechanisms of downstream extracellular matrix disruption in LPS-mediated preterm birth.
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