scholarly journals RASSF6 downregulation promotes the epithelial-mesenchymal transition and predicts poor prognosis in colorectal cancer

Oncotarget ◽  
2017 ◽  
Vol 8 (33) ◽  
pp. 55162-55175 ◽  
Author(s):  
Rui Zhou ◽  
Lin Qiu ◽  
Xiaolong Liu ◽  
Lijuan Ling ◽  
Ninglei Li ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition

scholarly journals Bioinformatic Analyses and Experimental Verification Reveal that High FSTL3 Expression Promotes EMT via Fibronectin-1/α5β1 Interaction in Colorectal Cancer

2021 ◽  
Vol 8 ◽  
Author(s):  
Yuanjie Liu ◽  
Jiepin Li ◽  
Shuhong Zeng ◽  
Ying Zhang ◽  
Yonghua Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Therapeutic Target ◽  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
Prognostic Biomarker ◽  
M2 Macrophages ◽  
Mesenchymal Transition ◽  
Prognostic Predictor ◽  
Potential Applications ◽  
Validation Experiments

Background: Colorectal cancer (CRC) is a typical cancer prevalent worldwide. Despite the conventional treatments, CRC has a poor prognosis due to relapse and metastasis. Moreover, there is a dearth of sensitive biomarkers for predicting prognosis in CRC.Methods: This study used a bioinformatics approach combining validation experiments to examine the value of follistatin-like 3 (FSTL3) as a prognostic predictor and therapeutic target in CRC.Results:FSTL3 was remarkably upregulated in the CRC samples. FSTL3 overexpression was significantly associated with a poor prognosis. FSTL3 was found to activate the epithelial-mesenchymal transition by promoting the binding of FN1 to α5β1. FSTL3 expression was also positively correlated with the abundance of the potent immunosuppressors, M2 macrophages.Conclusion:FSTL3 overexpression affects CRC prognosis and thus, FSTL3 can be a prognostic biomarker and therapeutic target with potential applications in CRC.

Epithelial mesenchymal transition in an advanced BRAF mutation type colorectal cancer.

2018 ◽  
Vol 36 (4_suppl) ◽  
pp. 693-693
Author(s):  
Jun-Eul Hwang ◽  
Woo Kyun Bae ◽  
Hyun-Jeong Shim ◽  
Sang-Hee Cho ◽  
Ik-Joo Chung
Keyword(s):  
Colorectal Cancer ◽  
Braf Mutation ◽  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
Disease Free Survival ◽  
Poor Overall Survival ◽  
Free Survival ◽  
Mesenchymal Transition ◽  
Disease Free ◽  
Mutation Type

693 Background: BRAF mutation is associated with poor survival in colorectal cancer. We aimed to generate genomic signature associated with BRAF mutation that possibly predict prognosis in colorectal cancer. Methods: A gene expression signature reflecting BRAF mutation was generated in TCGA cohorts (n = 207). The colorectal cancer patients were stratified into two groups according to this signature: BRAF mutation type colorectal cancer or BRAF wild type colorectal cancer. Prognostic significance of BRAF mutation-associated gene signature was tested in three independent cohorts (GSE 17536, GSE 14333, and GSE 39582). Results: The BRAF mutation signature was associated with poor prognosis in two independent cohorts (total n = 522). BRAF mutation type colorectal cancer was associated with poor disease-free survival (median: not reached, P = 0.0303) in GSE14333, and associated with poor overall survival (BRAF mutation vs. wild, P = 0.0355), poor disease-free survival (P = 0.00794), and poor disease-specific survival (P = 0.0341) in GSE 17536. In GSE 39582, BRAF mutation type colorectal cancer demonstrated the trend of poor overall survival according to increase of stage. In a multivariate analysis, BRAF mutation gene signature was independent poor prognostic factor for disease-free survival (hazard ratio 2.7; 95% CI 1.59-2.83: P = 0.001). Gene network analyses suggested epithelial-mesenchymal transition and colon cancer metastasis signaling are the possible explanations for poor prognosis of BRAF mutation type colorectal cancer. Conclusions: BRAF mutation signature is highly associated with poor prognosis in colorectal cancer, especially in advanced stage, and the molecules associated with epithelial-mesenchymal transition can be potential therapeutic targets in BRAF mutation type colorectal cancer.

ILEI: a novel marker for epithelial-mesenchymal transition and poor prognosis in colorectal cancer

2014 ◽  
Vol 65 (4) ◽  
pp. 527-538 ◽  
Author(s):  
Zhao-Hua Gao ◽  
Chong Lu ◽  
Zhen-Ning Wang ◽  
Yong-Xi Song ◽  
Jin-Liang Zhu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition

scholarly journals CYB5R1 links epithelial-mesenchymal transition and poor prognosis in colorectal cancer

Oncotarget ◽  
2016 ◽  
Vol 7 (21) ◽  
pp. 31350-31360 ◽  
Author(s):  
Christine Woischke ◽  
Cristina Blaj ◽  
Eva Marina Schmidt ◽  
Sebastian Lamprecht ◽  
Jutta Engel ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition

scholarly journals Hypomethylation of GDNF family receptor alpha 1 promotes epithelial-mesenchymal transition and predicts metastasis of colorectal cancer

PLoS Genetics ◽  
2020 ◽  
Vol 16 (11) ◽  
pp. e1009159
Author(s):  
Zhexu Dong ◽  
Lei Dai ◽  
Yong Zhang ◽  
Chao Fang ◽  
Gang Shi ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Early Diagnosis ◽  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
Dna Hypomethylation ◽  
Mesenchymal Transition ◽  
Akt Phosphorylation ◽  
Receptor Alpha

Tumor metastasis is the major cause of poor prognosis and mortality in colorectal cancer (CRC). However, early diagnosis of highly metastatic CRC is currently difficult. In the present study, we screened for a novel biomarker, GDNF family receptor alpha 1 (GFRA1) based on the expression and methylation data in CRC patients from The Cancer Genome Altlas (TCGA), followed by further analysis of the correlation between the GFRA1 expression, methylation, and prognosis of patients. Our results show DNA hypomethylation-mediated upregulation of GFRA1 in invasive CRC, and it was found to be correlated with poor prognosis of CRC patients. Furthermore, GFRA1 methylation-modified sequences were found to have potential as methylation diagnostic markers of highly metastatic CRC. The targeted demethylation of GFRA1 by dCas9-TET1CD and gRNA promoted CRC metastasis in vivo and in vitro. Mechanistically, demethylation of GFRA1 induces epithelial-mesenchymal transition (EMT) by promoting AKT phosphorylation and increasing c-Jun expression in CRC cells. Collectively, our findings indicate that GFRA1 hypomethylation can promote CRC invasion via inducing EMT, and thus, GFRA1 methylation can be used as a biomarker for the early diagnosis of highly metastasis CRC.

scholarly journals Correction to: The long non-coding RNA TUG1 indicates a poor prognosis for colorectal cancer and promotes metastasis by affecting epithelial-mesenchymal transition

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Junfeng Sun ◽  
Chaohui Ding ◽  
Zhen Yang ◽  
Tao Liu ◽  
Xiefu Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Non Coding Rna ◽  
Long Non Coding Rna

An amendment to this paper has been published and can be accessed via the original article.

scholarly journals Epithelial-Mesenchymal Transition and MicroRNAs in Colorectal Cancer Chemoresistance to FOLFOX

Pharmaceutics ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 75
Author(s):  
Paula I. Escalante ◽  
Luis A. Quiñones ◽  
Héctor R. Contreras
Keyword(s):  
Colorectal Cancer ◽  
Tumor Cells ◽  
Methylenetetrahydrofolate Reductase ◽  
Epithelial Mesenchymal Transition ◽  
Late Onset ◽  
Dihydropyrimidine Dehydrogenase ◽  
Acquired Resistance ◽  
Potential Effect ◽  
Mesenchymal Transition ◽  
Folfox Chemotherapy

The FOLFOX scheme, based on the association of 5-fluorouracil and oxaliplatin, is the most frequently indicated chemotherapy scheme for patients diagnosed with metastatic colorectal cancer. Nevertheless, development of chemoresistance is one of the major challenges associated with this disease. It has been reported that epithelial-mesenchymal transition (EMT) is implicated in microRNA-driven modulation of tumor cells response to 5-fluorouracil and oxaliplatin. Moreover, from pharmacogenomic research, it is known that overexpression of genes encoding dihydropyrimidine dehydrogenase (DPYD), thymidylate synthase (TYMS), methylenetetrahydrofolate reductase (MTHFR), the DNA repair enzymes ERCC1, ERCC2, and XRCC1, and the phase 2 enzyme GSTP1 impair the response to FOLFOX. It has been observed that EMT is associated with overexpression of DPYD, TYMS, ERCC1, and GSTP1. In this review, we investigated the role of miRNAs as EMT promotors in tumor cells, and its potential effect on the upregulation of DPYD, TYMS, MTHFR, ERCC1, ERCC2, XRCC1, and GSTP1 expression, which would lead to resistance of CRC tumor cells to 5-fluorouracil and oxaliplatin. This constitutes a potential mechanism of epigenetic regulation involved in late-onset of acquired resistance in mCRC patients under FOLFOX chemotherapy. Expression of these biomarker microRNAs could serve as tools for personalized medicine, and as potential therapeutic targets in the future.

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