MRNA microarray analysis in colorectal cancer tissues
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE212156 | GEO | 2025/08/26
REPOSITORIES: GEO
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2021-04-17 | GSE172229 | GEO
Project description:The incidence and mortality of colorectal cancer (CRC) is higher in African Americans (AAs) than in other ethnic groups in the U. S., but reasons for the disparities are unknown. We performed gene expression profiling and microsatellite instability (MSI) analysis of sporadic CRCs from AAs vs. European Americans (EAs) to assess the contribution to CRC disparities. We evaluated gene expression of 43 AA and 43 EA CRC tumors matched by stage and 40 normal colon tissues using the Agilent human whole genome 4x44K cDNA arrays. Gene and pathway analysis were performed using Significance Analysis of Microarrays (SAM), 10-fold Cross Validation (10-fCV) and Ingenuity Pathway Analysis (IPA). MSI analysis was assessed with five NIH Bethesda markers. SAM revealed that 95 genes were differentially expressed between AA and EA patients at a false discovery rate of <5%. A 10f-CV demonstrated that 9 genes were differentially expressed between AA and EA with an accuracy of 97%. Nine genes (CRYBB2, PSPH, ADAL, VSIG10L, C17orf81, ARSE, ANKRD36B, ZNF835, ARHGAP6) were validated and differential expression confirmed by qRT-PCR in independent test set of 21 patients (10 AA, 11 EA). We also analyzed MSI in 57 of the CRC subjects. Overall, 15.8% of CRC patients had MSI, with a higher rate observed in EA (20%) than in AA (12%). MSI distribution by tumor site was 77% right and 23% left colon. Previously, genetic, epigenetic and environmental factors have been implicated in the etiology of CRC. Our results are the first to implicate differential gene expression in CRC disparities and support the existence of distinct tumor microenvironments in these two patients' populations. 126 total samples: 1) 43 white cancer samples; 2) 43 black cancer samples; 3) 27 white control samples; 4) 13 black control samples.
2012-05-22 | E-GEOD-28000 | biostudies-arrayexpress
Project description:The incidence and mortality of colorectal cancer (CRC) is higher in African Americans (AAs) than in other ethnic groups in the U. S., but reasons for the disparities are unknown. We performed gene expression profiling and microsatellite instability (MSI) analysis of sporadic CRCs from AAs vs. European Americans (EAs) to assess the contribution to CRC disparities. We evaluated gene expression of 43 AA and 43 EA CRC tumors matched by stage and 40 normal colon tissues using the Agilent human whole genome 4x44K cDNA arrays. Gene and pathway analysis were performed using Significance Analysis of Microarrays (SAM), 10-fold Cross Validation (10-fCV) and Ingenuity Pathway Analysis (IPA). MSI analysis was assessed with five NIH Bethesda markers. SAM revealed that 95 genes were differentially expressed between AA and EA patients at a false discovery rate of <5%. A 10f-CV demonstrated that 9 genes were differentially expressed between AA and EA with an accuracy of 97%. Nine genes (CRYBB2, PSPH, ADAL, VSIG10L, C17orf81, ARSE, ANKRD36B, ZNF835, ARHGAP6) were validated and differential expression confirmed by qRT-PCR in independent test set of 21 patients (10 AA, 11 EA). We also analyzed MSI in 57 of the CRC subjects. Overall, 15.8% of CRC patients had MSI, with a higher rate observed in EA (20%) than in AA (12%). MSI distribution by tumor site was 77% right and 23% left colon. Previously, genetic, epigenetic and environmental factors have been implicated in the etiology of CRC. Our results are the first to implicate differential gene expression in CRC disparities and support the existence of distinct tumor microenvironments in these two patients' populations.
2012-05-23 | GSE28000 | GEO
Project description:Clinical Significance: Understanding the differences in colorectal cancer (CRC) aggressiveness and clinical outcomes in relation to tumor stage and different molecular subsets is at most important for designing treatment regimens. However, molecular signatures for specific phenotypic subsets that predict the aggressiveness and clinical outcomes of CRC, specifically in advanced disease stage are lacking. Therefore, for the first time, the current study has identified a set of molecular markers that are associated with aggressive Stage III CRCs that exhibited microsatellite stable and mutant p53 phenotypic features. These findings might aid in designing aggressive treatment regimens and help to provide insights into the development of novel therapeutic targets. Results: Increased incidence of p53 mutations in MSS CRCs (58%) was associated with higher CRC-specific mortality than MSS-p53 wild-type phenotypes (log-rank, P=0.025; and hazard ratio, 2.52; 95% confidence interval, 1.25-5.08). Of 49 down-regulated genes, LPAR6, PDLIM3 and PLAT and of 35 up-regulated genes, TRIM29, FUT3, IQGAP3, and SLC6A8, were confirmed by qNPA, qRT-PCR, and IHC platforms. Conclusions: p53 mutations are associated with poor prognosis of Stage III microsatellite stable CRCs. p53 wild type vs. mutant tumor samples
2012-01-26 | E-GEOD-27157 | biostudies-arrayexpress
Project description:Autophagy is activated in pancreatic ductal adenocarcinoma (PDAC) and is currently being considered a promising therapeutic target in clinical trials. PDAC is a highly lethal disease with incidence rate equalling mortality rate. Main reasons for PDAC lethality are late-stage diagnosis, high agressiveness and metastatic rate, lack of effective treatments as well as specific diagnostic markers. Here we show that varying levels of the Autophagy related gene 5 (Atg5) determine pancreatic tumor formation and malignancy. While homozygous deletion of Atg5 blocks tumor progression in an in vivo model of PDAC, heterozygous deletion increases tumor aggressiveness and metastasis. Further analyses reveal that monoallelic loss of Atg5 affects mitochondrial homeostasis, changes intracellular calcium oscillations, heightens extracellular cathepsin activities , and promotes a pro-tumorigenic inflammatory microenvironment collectively enhancing tumor cell migration, invasion, and metastasis. Future treatments should take into account that variations in the autophagy pathway may have opposing effects on pancreatic tumor load, especially considering the multitude of autophagy inhibitors currently tested in clinical trials.
2018-10-15 | E-MTAB-6275 | biostudies-arrayexpress
Project description:Abstract Background:Colorectal Cancer (CRC) is a common malignant tumor of the digestive tract, with poor prognosis in advanced stages due to metastasis and immune evasion.Chronic intestinal inflammation may promote CRC progression by inducing an imbalance in the immune microenvironment, thus therapeutic strategies targeting immune regulation urgently need to be explored.Wumei Wan (WMW), a traditional Chinese herbal formula, has shown marked anti-inflammatory activity in ulcerative colitis (UC).However, whether it can inhibit CRC progression remains unclear. Aim:This study aims to investigate whether WMW can ameliorate CRC and to explore its underlying mechanisms. Methods:An AOM/DSS-induced CRC mouse model was established, and transcriptomicss, metabolomics, and network pharmacology analyses were integrated to investigate and validate the mechanisms of WMW. Results:WMW ameliorated CRC progression by improving colonic pathological conditions, lowering Disease Activity Index (DAI) scores, enhancing survival, and suppressing tumor growth in CRC mice. Specifically, the WMW group’s DAI score decreased by approximately 34.36% compared to the model group. Additionally, by day 70, the survival rate in the WMW-treated group was 22.806% higher than that of the model group. Multi-omics and network pharmacology analyses indicated that WMW inhibited the IDO-Kyn-AHR signaling pathway, decreased Th17 and Treg cell proliferation and differentiation, restored CD8+T cell function, and enhanced antitumor immunity. Conclusion：This research demonstrates for the first time that WMW suppresses CRC progression by rebalancing Th17/Treg immunity through modulation of the IDO1-Kyn-AHR pathway.
2025-07-16 | GSE295477 | GEO
Project description:Colorectal cancer (CRC) is a major cause of cancer mortality and a serious health concern worldwide. Vitamin D deficiency is associated with high CRC incidence and mortality, suggesting a protective effect of vitamin D against this neoplasia. Although the antiproliferative and prodifferentiation action of active vitamin D (1alpha,25-dihydroxyvitamin D3, 1,25(OH)2D3) on colon carcinoma cells is well documented, its potential effects on CRC stroma are unknown. Here, we show that high vitamin D receptor (VDR) expression in tumor stromal fibroblasts is associated with better overall and progression-free survival in a large cohort of CRC patients, irrespective of its expression in carcinoma cells. Consistently, 1,25(OH)2D3 inhibits the activation of patient-derived normal and cancer-associated fibroblasts, and their pro-migratory effect on carcinoma cells. Importantly, we show by global transcriptomic analyses that 1,25(OH)2D3 regulates cancer-associated fibroblast gene expression and imposes a gene signature that is associated with longer overall and disease-free survival of CRC patients. Moreover, expression of two genes from the signature, CD82 and S100A4, correlates with stromal VDR expression and clinical outcome in CRC. This study provides the first evidence that vitamin D has protective effects against CRC through the regulation of stromal fibroblasts. Characterization of 1,25(OH)2D3 action on gene expression in primary cultures of colon normal and tumor fibroblasts established from samples from colorectal cancer patients. RNA from seven paired normal and tumor fibroblast primary cultures treated with 1,25(OH)2D3 or vehicle for 48 h were analyzed.
2016-04-07 | E-GEOD-70468 | biostudies-arrayexpress
Project description:Colorectal cancer (CRC) with high rate of mortality is one of the most commonly diagnosed cancers in worldwide. Advanced colorectal cancer is often accompanied by malignant proliferation of tumor cells. Further researches on colorectal cancer proliferation to find new targets and develop new therapeutic regimen are an important direction for colorectal cancer treatment. In this study, genome-wide RNAi screening was used to discover the essential genes associated with colorectal cancer cell proliferation. We found DKC1 (dyskerin pseudouridine synthase 1) promoted CRC proliferation through binding and modifying ribosomal proteins (RPL10A, RPL22L1, RPL34, RPS3) mRNA to increase the mRNAs stability and eventually increasing their expression. Besides, DKC1 is highly expressed in colorectal cancer and its aberrantly high expression is associated with poor prognosis of colorectal cancer patients. These results suggest that DKC1 could be a new therapeutic target for colorectal cancer.
2021-02-08 | PXD018103 | Pride
Project description:Background: Colorectal cancer (CRC) remains the second leading cause of cancer mortality in the U.S., with significant racial and ethnic disparities in incidence, survival, and mortality rates. The rising incidence of early-onset CRC and the frequent presentation at advanced stages of CRC among the Hispanics makes this an important ethnic group to study. A deeper understanding of the complex interplay between molecular, genetic, and environmental factors is critical for developing targeted therapies to reduce the prevalence in specific racial and ethnic groups, such as Hispanics. This study explores the role of stress-survival pathway (SSP) genes in early-onset and late-stage CRC, primarily focusing on disparities between Hispanics and Non-Hispanic Whites (NHWs). Additionally, this study investigates the role of MCM10, in contributing to CRC disparities among the Hispanic populations with an emphasis of early-onset and late-stage CRC Hispanics. Methods: One of our previous studies had identified some SSP protein coding genes associated with CRC. The expressions of these genes were validated in CRC cell lines, cDNA arrays, tissue microarrays, and tissue samples using qRT-PCR, and immunohistochemistry. The transcript-level expressions of differentially expressed SSP genes were further evaluated in Hispanic and NHWs tumor tissues, including early onset and late-stage cohorts. Additionally, we performed cellular physiological and functional assays to explore the role of MCM10 in tumor progression, before and after siRNA mediated knockdown. High-throughput transcriptomic and proteomic analyses were performed to reveal the underlying molecular mechanism. Results: We observed differential expressions of twelve SSP genes in CRC cell lines, at the transcript level; that of ten genes in early and late stages using cDNA arrays, and nine genes at the protein levels using tissue microarrays and immunohistochemistry. Hispanic CRC samples showed differential expression of all nine SSP genes compared to NHWs, in early-onset, and late-stage CRC, with all genes being upregulated other than CDK4 and PRDX4 in late-stage CRC and CDK4 in early-onset CRC. Our functional study demonstrated that MCM10 knockdown in CRC cell lines significantly reduced cell proliferation, growth, invasion and migration by inducing cell cycle arrest, apoptosis and reactive oxygen species pathways. The integrative RNA-sequencing and proteomics study reported that the novel gene PPFI1A could be associated with MCM10 mediated cancer progression. The role of MCM10 and PPFI1A in cancer progression has been validated using a Hispanic CRC patient derived organoid. Conclusion: This study highlights the role of SSP genes, particularly MCM10, in colorectal cancer progression and its potential as a biomarker and therapeutic target to address Hispanic CRC disparities.
2025-08-06 | GSE304110 | GEO
Project description:Colorectal cancer (CRC) with high rate of mortality is one of the most commonly diagnosed cancers in worldwide. Advanced colorectal cancer is often accompanied by malignant proliferation of tumor cells. Further researches on colorectal cancer proliferation to find new targets and develop new therapeutic regimen are an important direction for colorectal cancer treatment. In this study, genome-wide RNAi screening was used to discover the essential genes associated with colorectal cancer cell proliferation. We found DKC1 (dyskerin pseudouridine synthase 1) promoted CRC proliferation through binding and modifying ribosomal proteins (RPL10A, RPL22L1, RPL34, RPS3) mRNA to increase the mRNAs stability and eventually increasing their expression. Besides, DKC1 is highly expressed in colorectal cancer and its aberrantly high expression is associated with poor prognosis of colorectal cancer patients. These results suggest that DKC1 could be a new therapeutic target for colorectal cancer.
2021-04-30 | GSE147348 | GEO