RNA-seq analysis on primary tumor and liver metastatic lesion of CRC
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE179979 | GEO | 2021/12/31
REPOSITORIES: GEO
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Project description:RNA-seq analysis on primary tumor and liver metastatic lesion of CRC
| PRJNA746129 | ENA
Project description:We carried out comprehensive analysis for the miRNA profiling of primary tumor and metastatic lesion which seems to be source of circulating miRNA. We picked up two patients who treated with primary tumor resection initially and received chemotherapy followed by surgical resection of liver metastasis. The total miRNA was isolated from frozen tissue specimens. SurePrint G3 Human miRNA microarray kit Rel.21.0 (Agilent Technologies) contains 2549 human microRNA probes. As previously reported, hsa-miR200c revealed specifically high expression in metastatic sites at both two cases. In two colorectal cancer patients, the frozen primary tumor, normal mucosa and liver-metastatic lesion were analyzed by microRNA microarray.
2015-09-19 | E-GEOD-73178 | biostudies-arrayexpress
Project description:The purpose of this study is to identify lncRNAs involved in the pathology of colorectal cancer (CRC) liver metastasis and investigate their underlying mechanisms. A total of 439 miRNAs were identified to be differentially expressed between 7 primary CRC tissues with liver metastases and 8 CRC tissues without liver metastases from 15 patients by Arraystar lncRNA microarrays
2017-02-28 | GSE95423 | GEO
Project description:Using liver metastases from 4 colorectal cancer patients (CRC-LM), we explored one receptor: EGFR whose signaling triggers cell proliferation and is exacerbated in many tumors.
2023-06-14 | GSE217414 | GEO
Project description:We present a novel approach for investigating transcriptomic differences between primary colorectal cancers (CRC) and distant CRC metastases, which may help to identify primaries at high risk for future dissemination and to inform the development of metastasis-targeted therapies. Eliminating tissue specificity of the “host” organs where tumors are located and adjusting for confounders such as exposure to chemotherapy and radiation, allows for an effective comparison of primary CRC and metastatic lesion transcriptomes at both the gene and pathway levels. Using this approach, our discovery-validation design identified that metastases are characterized by reduced epithelial-mesenchymal-transition (EMT) but increased MYC target and DNA repair pathway activities. The most significant gene-level expression differences between primaries and metastases were in FBN2 and MMP3, which showed over a 7-fold difference. In addition, we uncovered two distinct subtypes of CRC metastases that are characterized by either EMT-inflammatory or proliferative phenotypes, and demonstrated that none of the metastases examined were of consensus molecular subtype (CMS) 3 suggesting subtype exclusivity. Highlighting transcriptome differences between primary tumors and CRC metastases delineates pathways that may be activated in metastases and may assist in the development and/or selection of existing targeted treatment regimens for individuals with metastatic disease.
2019-05-18 | GSE131418 | GEO
Project description:In this study, we conducted a microarray-based analysis to identify differentially expressed miRNAs in CRC by comparing miRNA profiles among primary CRC tissues from patients with liver metastases, primary tissues without liver metastases, and liver metastatic lesions. microRNAs (miRNAs) have been shown to have a potential for cancer diagnosis lately. The main objective of this study is to identify a novel biomarker serum miRNA from the patients with colorectal cancer (CRC). Microarray analysis of miRNA expression was performed using paired pre- and post- operative serum from 10 CRC patients. Two miRNAs (let-7a, miR-199a-3p) decreased significantly in the post-operative serum when compared to pre-operative serum (P=0.015 and 0.029, respectively). Microarrays were performed for the testing cohort of primary CRC lesions (n=28) and liver metastatic lesions (n=8).
2016-02-14 | E-GEOD-72199 | biostudies-arrayexpress
Project description:Colon and liver have an inseparable relationship since embryological development. More than half of colorectal cancer patients developed liver metastases accompanied with poor prognosis. Recent evidence suggests that distant metastatic organs are “educated” by primary tumor-derived extracellular vesicles. Here we found that the liver-specific pro-metastatic effect of colorectal cancer (CRC)-derived small extracellular vesicles (sEVs). In vivo experiments showed that the injected fluorescence-labeled CRC-derived sEVs were accumulated and taken up by macrophages in the mouse liver. MicroRNA sequencing revealed the highest expression of microRNA (miR)-21-5p in CRC-derived sEVs. In vitro co-culture experiments showed that the sEVs polarized macrophages toward an interleukin-6(IL-6)-secreting type of macrophages. Further mouse experiments and microarray studies indicated that the CRC-sEVs increased macrophage invasion and induced an inflammatory microenvironment in the liver, which promoted liver metastasis of orthotropic- transplanted CRC cells. Most importantly, the TCGA data analysis and clinical sample examinations demonstrated that miR-21-5p expressions were sharply raised in the CRC tissues. We apply Tethered Cationic Lipoplex Nanoparticles (tCLN) technology in detecting CRC patients’ sEVs miR-21 in plasma and found strong correlation between sEVs-miR-21 and CRC liver metastasis. The serum IL-6 level was much higher in CRC patients with liver metastasis, and the liver metastasis relevance of MiR-21, macrophages, and IL-6 in CRC patients. Thus, we propose the role of CRC-derived sEVs in the formation of an inflammatory pre-metastatic niche in liver for CRC metastasis through macrophage polarization via a miR-21/TLRs pro-inflammation pathway.
2019-07-01 | GSE100435 | GEO
Project description:Background: In vitro models are an essential tool towards understanding the molecular characteristics of colorectal cancer (CRC) and the testing of therapies for CRC. To this end we established 21 novel CRC cell lines of which six were derived from liver metastases. Extensive genetic, genomic, transcriptomic and methylomic profiling was performed in order to characterize these new cell lines and all data is made publically available. Additionally, sensitivity of oxaliplatin was tested as a measure for chemotherapy resistance. Results: DNA copy-number alterations (CNA) were compared between primary and metastasis derived cell lines. In concordance with previous studies copy-number gain of chr20, and loss of chr8p were found highly specific for liver metastases. Previously reported BRAF-mutation associated DNA methylation profiles could be validated on the genome-wide DNA methylation profiles of these cell lines. 47.6% of the loci previously reported to associate with BRAF mutation status were reproduced in this dataset. When examining the gene expression profiles in conjunction with these DNA methylation results, we identified 20 genes of which the gene expression correlated with the DNA methylation status, including MEIS1, LRAT and STC2. These genes have previously been reported to be subject to transcriptional regulation through DNA hypermethylation, validating our approach. Conclusions: By combining mutation profiles with CNA and gene expression profiles we constructed an overview of the alterations in the major CRC-related signalling pathways. The mutation profiles, along with the genome, transcriptome and methylome data of these cell lines will be made publically available . This combined dataset puts these cell lines among the best characterized CRC cell lines, allowing researchers to select appropriate cell line models for their particular experiment, making optimal use of these novel cell lines as in vitro model for CRC. 21 CRC cell lines were analyzed
2016-02-29 | E-GEOD-67772 | biostudies-arrayexpress
Project description:About 50% of colorectal cancer patients develop liver metastases. Patients with metastatic colorectal cancer have 5-year survival rates below 20% despite new therapeutic regimens. Tumor heterogeneity has been linked with poor clinical outcome, but was so far mainly studied via bulk genomic analyses. In this study we performed spatial proteomics via MALDI mass spectrometry imaging on six patient matched CRC primary tumor and liver metastases to characterize interpatient, intertumor and intratumor hetereogeneity. We found several peptide features that were enriched in vital tumor areas of primary tumors and liver metastasis and tentatively derived from tumor cell specific proteins such as annexin A4 and prelamin A/C. Liver metastases of colorectal cancer showed higher heterogeneity between patients than primary tumors while within patients both entities show similar intratumor heterogeneity sometimes organized in zonal pattern. Together our findings give new insights into the spatial proteomic heterogeneity of primary CRC and patient matched liver metastases.
2023-02-17 | PXD039409 | Pride
Project description:Colorectal cancer is one of the most frequently occurring malignancies and a major cause of cancer death. Distant metastases in this disease most commonly develop in the liver and are often untreatable. Here, we show that citrullination of the extracellular matrix (ECM) by cancer cell derived peptidylarginine deiminase 4 (PAD4) is essential for the growth of liver metastases. Citrullination of proteins, a post-translational conversion of arginine residues to citrulline, is well recognized in rheumatoid arthritis, but largely undocumented in cancer. PAD4, a key enzyme responsible for catalyzing citrullination, is produced by metastatic colorectal cancer cells and found at higher levels in human liver metastases than in normal liver. Functional significance for citrullination in metastatic growth was evident in murine models where inhibition of citrullination, either globally by pharmacologic inhibition of PADs or specifically in colorectal cancer cells by PAD4 knockdown substantially reduced liver metastatic burden. Additionally, citrullination of a key ECM component collagen type I led to greater adhesion and decreased migration of colorectal cancer cells along with increased expression of characteristic epithelial markers, suggesting a role for citrullination in promoting mesenchymal-to-epithelial transition (MET) and liver metastasis. Overall, our study revealed the potential for PAD4-dependant citrullination to drive the progression of liver metastasis. These data indicate that inhibition of citrullination could be exploited to prevent the development of liver metastases in colorectal cancer.
2018-10-18 | PXD010252 | Pride