Browse
Submit Data
Databases
API
Help

Dataset Information

6 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Increased Collagen Type V α2 (COL5A2) in Colorectal Cancer is Associated with Poor Prognosis and Tumor Progression.

ABSTRACT:

Purpose

Colorectal cancer (CRC) is the third most common cancer in males and the second in females worldwide with very poor prognosis. Extracellular matrix proteins like collagens play important roles in cancer progression. Collagen type V α2 (COL5A2) is increased in several cancers but its role in cancer remains unclear.

Methods

COL5A2 expression was evaluated by interrogation of public Oncomine gene microarray datasets and immunohistochemistry (IHC) analyses of two tissue microarrays containing 180 paired CRC cases. Survival analysis was performed using Kaplan-Meier survival curve and Cox proportional hazards regression methods. COL5A2 was ectopically expressed in CRC cells, and the cell proliferation was measured using the methylthiazolyldiphenyl-tetrazolium bromide (MTT) method.

Results

COL5A2 gene was significantly upregulated in the most types of CRC comparing with the normal counterparts. The mRNA expression of COL5A2 was associated with cancer stages, gender, recurrence, microsatellite instability and KRAS status of CRC. COL5A2 protein increased in the cancer epithelial cells comparing with the normal counterpart and associated with age and T stage of CRC, whereas stromal expression of COL5A2 has no significant change between cancerous and normal tissues. COL5A2 gene and protein (epithelial expression) are independent risk factors and predict poor prognosis of CRC. Ectopic expression of COL5A2 drives colon cancer cell growth and upregulates WNT/β-catenin and PI3K/mTOR signaling via binding DDR1.

Conclusion

COL5A2 is a potential prognostic marker of CRC.

SUBMITTER: Wang J

PROVIDER: S-EPMC8107053 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

High expression of CDCA7 predicts tumor progression and poor prognosis in human colorectal cancer.

Project description:Colorectal cancer (CRC) is one of the most fatal types of cancer worldwide. This study aimed to determine the predictive and prognostic values of cell division cycle associated protein 7 (CDCA7) in CRC. Firstly, the relationship between CDCA7 and CRC was assessed through bioinformatics analysis. Subsequently, CDCA7 expression levels were detected in various CRC cell lines, as well as 15 fresh human CRC tissues and their paired adjacent normal colorectal tissues using reverse transcription‑quantitative PCR and western blotting. Additionally, immunohistochemical staining was used to determine the levels of CDCA7 in 104 CRC tissues and their paired adjacent normal colorectal tissues. The present study revealed that CDCA7 expression was upregulated in CRC tissues and cell lines. The positive expression rates of CDCA7 in normal and CRC tissues were 26.92 and 75.96%, respectively. The intensities of CDCA7 immunostaining were significantly associated with CRC invasion depth, lymph node metastasis, tumor‑node‑metastasis stage and distant metastasis. However, no significant differences in sex, age, tumor size and CRC differentiation were found between high and low CDCA7 expression groups. Furthermore, patients with low CDCA7 expression exhibited a greater overall survival rate of CRC compared to those with high CDCA7 expression. The findings of this study indicated that CDCA7 may serve a significant role in CRC prognosis and progression, and may be considered a novel biomarker for the prediction of patient survival after colectomy.

| S-EPMC7248471 | biostudies-literature

A five-gene signature is associated with tumor progression and poor prognosis in colorectal cancer

Project description:We developed an experimentally derived molecular signature from mouse tumor models that is closely associated with survival of colorectal cancer (CRC) patients. We isolated single cell-derived progenies (SCPs) from the SW480 CRC cell line and compared their metastatic potential in an orthotopic implantation model of murine CRC. We compared the differences in the gene expression profiles of a high metastatic variant SCP51, a low metastatic variant SCP58 and their parent SW480/EGFP.

2011-08-31 | E-GEOD-16934 | biostudies-arrayexpress

Downregulation of DUSP9 Promotes Tumor Progression and Contributes to Poor Prognosis in Human Colorectal Cancer.

Project description:BackgroundDual-specificity phosphatase 9 (DUSP9) belongs to the dual-specificity protein phosphatase subfamily. Recently, increasing attention has been paid on the role of DUSP9 in a variety of cancers. However, its functional role in tumor development is still unclear, especially in colorectal cancer (CRC).MethodsThe functional role of DUSP9 in inhibiting the progression of CRC was verified using colony formation assay, wound healing assay, nude mice xenograft model, etc. RNA-seq was performed to assess the gene expression profiling in SW480 cells with DUSP9 stable knockdown and shControl cells. Bisulfite sequencing (BSE) was performed to reveal the methylation status of CpG island in the promoter of DUSP9.ResultsDUSP9 was significantly downregulated in tumor tissues compared with peritumor tissues. Mechanistically, the high methylation status of CpG island in the promoter of DUSP9 may lead to the downregulation of DUSP9 in CRC. Clinically, low DUSP9 expression in CRC was closely associated with depth of invasion, metastasis (TNM) stage, and poor survival, indicating that DUSP9 may be involved in the progression of CRC. Functional study revealed that DUSP9 inhibited proliferation, migration, invasion, and epithelial-mesenchymal transition of CRC cells both in vitro and in vivo. Transcriptome profiling studies revealed that Erk signaling was involved in the tumor progression mediated by DUSP9 silencing, which is confirmed by cell experiments and clinical tissue sample staining analysis.ConclusionOur findings demonstrate that DUSP9 plays a critical role in the progression of CRC, and therapeutic intervention to increase the expression or activity of DUSP9 may be a potential target for CRC treatment in the future.

| S-EPMC7538709 | biostudies-literature

A five-gene signature is associated with tumor progression and poor prognosis in colorectal cancer

Project description:We developed an experimentally derived molecular signature from mouse tumor models that is closely associated with survival of colorectal cancer (CRC) patients.

2011-09-01 | GSE16934 | GEO

UBN2 promotes tumor progression via the Ras/MAPK pathway and predicts poor prognosis in colorectal cancer.

Project description:BackgroundUbinuclein-2 (UBN2) is a nuclear protein that interacts with many transcription factors. The molecular role and mechanism of UBN2 in the development and progression of cancers, including colorectal cancer (CRC), is not well understood. The current study explored the role of UBN2 in the development and progression CRC.MethodsOncomine network and The Cancer Genome Atlas (TCGA) database were downloaded and Gene Set Enrichment Analysis (GSEA) was performed to compare the UBN2's expression between normal and tumor tissues, as well as the potential correlation of UBN2 expression with signaling pathways. Immunohistochemistry (IHC), qRT-PCR and Western blotting were performed to determine the expression of UBN2 in CRC tissues or cell lines. In vitro proliferation and invasion assays, and orthotopic mouse metastatic model were used to analyze the effect of UBN2 on the development and progression of CRC.ResultsThe analysis of UBN2 expression using Oncomine network showed that UBN2 was upregulated in CRC tissues compared to matched adjacent normal intestinal epithelial tissues. IHC, qRT-PCR and Western blotting confirmed that UBN2 expression is higher in CRC tissues compared with matched adjacent normal intestinal epithelial tissues. In addition, analyses of TCGA data revealed that high UBN2 expression was associated with advanced stages of lymph node metastasis, distant metastasis, and short survival time in CRC patients. IHC showed that high UBN2 expression is correlated with advanced stages of CRC. Moreover, UBN2 is highly expressed in the liver metastatic lesions. Furthermore, knockdown of UBN2 inhibited the growth, invasiveness and metastasis of CRC cells via regulation of the Ras/MAPK signaling pathway.ConclusionThe current study demonstrates that UBN2 promotes tumor progression in CRC. UBN2 may be used as a promising biomarker for predicting the prognosis of CRC patients.

| S-EPMC6511126 | biostudies-literature

Overexpression of CHKA contributes to tumor progression and metastasis and predicts poor prognosis in colorectal carcinoma.

Project description:Aberrant expression of choline kinase alpha (CHKA) has been reported in a variety of human malignancies including colorectal carcinoma (CRC). However, the role of CHKA in the progression and prognosis of CRC remains unknown. In this study, we found that CHKA was frequently upregulated in CRC clinical samples and CRC-derived cell lines and was significantly correlated with lymph node metastasis (p = 0.028), TNM stage (p = 0.009), disease recurrence (p = 0.004) and death (p < 0.001). Survival analyses indicated that patients with higher CHKA expression had a significantly shorter disease-free survival (DFS) and disease-specific survival (DSS) than those with lower CHKA expression. Multivariate analyses confirmed that increased CHKA expression was an independent unfavorable prognostic factor for CRC patients. In addition, combination of CHKA with TNM stage was a more powerful predictor of poor prognosis than either parameter alone. Functional study demonstrated that knockdown of CHKA expression profoundly suppressed the growth and metastasis of CRC cells both in vitro and in vivo. Mechanistic investigation revealed that EGFR/PI3K/AKT pathway was essential for mediating CHKA function. In conclusion, our results provide the first evidence that CHKA contributes to tumor progression and metastasis and may serve as a novel prognostic biomarker and potential therapeutic target in CRC.

| S-EPMC5341828 | biostudies-literature

Increased long noncoding RNA SNHG20 predicts poor prognosis in colorectal cancer.

Project description:Long noncoding RNAs (lncRNAs) have been suggested to be involved in the development and progression of malignancies. However, the investigation of small nucleolar RNA host gene 20 (SNHG20) on cancer progression remains unknown. The present study aims to explore the clinical significance of SNHG20 and its potential molecular mechanism in colorectal cancer (CRC).Quantitative real-time PCR (qRT-PCR) was used to measure the SNHG20 expression in a total of 107 CRC tissues and CRC cell lines. Loss of function approach was employed to explore the biological roles of SNHG20 in vitro. Its potential molecular mechanism was further verified by western blotting and qRT-PCR.The results suggested that SNHG20 expression was significantly upregulated in CRC tissues compared to corresponding normal tissues from 107 CRC patients. High expression of SNHG20 was remarkably associated with advanced TNM stage in patients with CRC. Multivariate analyses unraveled that SNHG20 expression was an independent prognostic factor for overall survival in CRC patients. Further functional assays revealed that knockdown of SNHG20 suppressed cell proliferation, invasion and migration, and cell cycle progression in CRC cells. Moreover, SNHG20 regulated cell growth through modulation of a series of cell cycle-associated genes.Our findings suggest that dysregulation of SNHG20 participates in CRC progression and may serve as a potential therapeutic target in CRC patients.

| S-EPMC4992210 | biostudies-literature

Increased levels of LAPTM4B, VEGF and survivin are correlated with tumor progression and poor prognosis in breast cancer patients.

Project description:This study explored the relationships among the expression of LAPTM4B, VEGF, and survivin and clinicopathological characteristics and prognosis in breast cancer patients.The expression of these three molecules in 110 stage I-III breast cancer patients with clinicopathological and follow-up data was detected via immunohistochemistry. Kaplan-Meier and Cox proportional hazard regression analyses were performed to assess the prognostic significance of these markers in breast cancer. Moreover, expression levels of these markers were evaluated in 5 breast cell lines via Western blot analysis.LAPTM4B, VEGF, and survivin were over-expressed in breast cancer specimens and highly expressed in MDA-MB-231 cells. VEGF and nuclear survivin expression was significantly correlated with LAPTM4B expression, and high levels of all three were associated with a tumor size >2cm, TNM stage II+III and lymph node metastasis, which had worse impacts on overall survival and progression-free survival in breast cancer patients. A multivariate Cox analysis identified LAPTM4B over-expression as an independent prognostic marker in breast cancer.These findings suggest that LAPTM4B, VEGF, and nuclear survivin expression are significantly correlated in breast cancer, which may be predictive of prognosis as well as effective therapeutic targets for new anticancer therapies.

| S-EPMC5522199 | biostudies-other

Increased <i>ATP2A1</i> Predicts Poor Prognosis in Patients With Colorectal Carcinoma.

Project description:Colorectal cancer is one of the most common malignant tumors in the digestive system. Traditional diagnosis and treatment methods have not significantly improved the overall survival of patients. In this study, we explored the value of ATP2A1 as a biomarker in predicting the prognosis of colorectal cancer patients. We used the TCGA database to reveal the relationship between ATP2A1 mRNA level and prognosis, methylation, and immune invasion in colorectal cancer. The results showed that the expression of ATP2A1 was increased in colorectal cancer. The overall survival of patients with high expression of ATP2A1 was significantly lower than patients with low expression of ATP2A1. Cox regression analysis showed that high expression of ATP2A1 was an independent risk factor for poor prognosis in colorectal cancer patients. In addition, we used three datasets to perform a meta-analysis, which further confirmed the reliability of the results. Furthermore, we revealed that ATP2A1 could significantly inhibit the proliferation of colorectal cancer cells by inhibiting the autophagy process and was associated with several immune cells, especially CD8 + T cells. Finally, four small molecule drugs with potential inhibition of ATP2A1 expression were found by CMap analysis. This study demonstrates for the first time that ATP2A1 is a potential pathogenic factor, which may play a significant role in colorectal cancer.

| S-EPMC9243465 | biostudies-literature

Overexpression of PLOD3 promotes tumor progression and poor prognosis in gliomas.

Project description:High-grade gliomas are the most threatening brain tumors due to aggressive proliferation and poor prognosis. Thus, utilizing genetic glioma biomarkers to forecast prognosis and guide clinical management is crucial. Procollagen-lysine, 2-oxoglutarate 5-dioxygenase 3 (PLOD3) modulates cancer progression and metastasis. However, its detailed function in cancer remains largely uninvestigated. PLOD3 expression was evaluated with real-time PCR in glioblastoma (GBM) cell lines and by Gene Expression Omnibus dataset analysis and immunohistochemistry of glioma tissues. We investigated the clinical use of PLOD3 for determining glioma prognosis. The biological roles of PLOD3 in proliferation, migration and invasion of GBM cells were studied both in vitro with wound-healing and transwell assays and in vivo using an orthotopic xenograft mouse model. Hypoxia and western blotting were applied to discover the molecular mechanisms underlying PLOD3 functions. PLOD3 mRNA and protein expression were upregulated in glioma tissues compared to normal brain tissues. PLOD3 overexpression was correlated with negative survival in glioma patients. PLOD3 silencing suppressed cell proliferation and induced G1 phase arrest through p53-independent regulation of the p21 pathway. Inhibition of PLOD3 in glioma cells decreased VEGF expression, migration and invasion by downregulating mesenchymal markers, including Snail and Twist. Notably, knockdown of PLOD3 inhibited HIF-1? accumulation via the ERK signaling pathway under hypoxia. Taken together, these discoveries reveal that PLOD3 is a potential therapeutic target in human gliomas.

| S-EPMC5884658 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data