Identification of genomic expression differences between right-sided and left-sided colon cancer based on bioinformatics analysis

Peng, Qiliang; Lin, Kaisu; Chang, Tao; Zou, Li; Xing, Pengfei; Shen, Yuntian; Zhu, Yaqun

doi:10.2147/ott.s154207

Cited by 14 publications

(13 citation statements)

References 43 publications

(39 reference statements)

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“…Various studies have provided evidence of remarkable molecular diversities between right-sided and left-sided colon cancer. Thus, an initial study by Yamauchi et al provided evidence that the frequency of CIMP-high, MSI-high and BRAF mutations gradually increased from rectum to ascending colon; in contrast, the frequency of KRAS mutations remained relatively stable at various tumor sites [ 97 , 234 ]. Sincrope et al confirmed a higher frequency of BRAF -mutated tumors among proximal colon cancers and also showed that mutation in KRAS codon 12 was more frequent in normal tumors, while non-mutated BRAF/KRAS was increased in distal tumors [ 235 ].…”

Section: Somatic Genetic Abnormalities In Colon Cancermentioning

confidence: 99%

Colorectal Cancer: Genetic Abnormalities, Tumor Progression, Tumor Heterogeneity, Clonal Evolution and Tumor-Initiating Cells

2018

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Colon cancer is the third most common cancer worldwide. Most colorectal cancer occurrences are sporadic, not related to genetic predisposition or family history; however, 20–30% of patients with colorectal cancer have a family history of colorectal cancer and 5% of these tumors arise in the setting of a Mendelian inheritance syndrome. In many patients, the development of a colorectal cancer is preceded by a benign neoplastic lesion: either an adenomatous polyp or a serrated polyp. Studies carried out in the last years have characterized the main molecular alterations occurring in colorectal cancers, showing that the tumor of each patient displays from two to eight driver mutations. The ensemble of molecular studies, including gene expression studies, has led to two proposed classifications of colorectal cancers, with the identification of four/five non-overlapping groups. The homeostasis of the rapidly renewing intestinal epithelium is ensured by few stem cells present at the level of the base of intestinal crypts. Various experimental evidence suggests that colorectal cancers may derive from the malignant transformation of intestinal stem cells or of intestinal cells that acquire stem cell properties following malignant transformation. Colon cancer stem cells seem to be involved in tumor chemoresistance, radioresistance and relapse.

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Section: Somatic Genetic Abnormalities In Colon Cancermentioning

confidence: 99%

Colorectal Cancer: Genetic Abnormalities, Tumor Progression, Tumor Heterogeneity, Clonal Evolution and Tumor-Initiating Cells

2018

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“…During tumor metastasis, epithelial mesenchymal transmission (EMT) is considered a vital process during which epithelial cells lose cellular polarity and cell-cell adhesion, and are transformed into separable and aggressive mesenchymal cells. 3 EMT is controlled by numerous growth factors and dissimilar factors, including Wnt, TGF-β, Notch and tyrosine kinase receptor. 4 The activation and initiation of these signaling pathways result in transcriptional suppression of numerous target genes which are involved in the loss functional activity of E-cadherin, which is a renowned marker of EMT.…”

Section: Introductionmentioning

confidence: 99%

Down-regulation of CXCL 11 inhibits colorectal cancer cell growth and epithelial-mesenchymal transition

Gao¹,

Liu²,

Li³

et al. 2018

OTT

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BackgroundThe poor prognosis of colorectal cancer (CRC) largely results from local invasion and tumor metastases. Epithelial-mesenchymal transition (EMT) is a key step in the progression of solid tumors and plays a vital role in tumor metastasis. Recent studies demonstrate that C-X-C motif chemokine 11 (CXCL11) is involved in various cancers’ progression. However, its biological activity in CRC needs deeper exploration.MethodsThe level of CXCL11 in CRC tissues and cell lines was determined using the quantitative real-time PCR (qRT-PCR) assay. The MTT, colony formation, wound healing and Transwell invasion assays were applied to assess the role of CXCL11 in CRC cell growth, migration and invasion, in vitro, respectively. A xenograft model was constructed to analyze the function of CXCL11 in CRC cell growth in vivo.ResultsCXCL11 was over-expressed in CRC tissues and cell lines. Repression of CXCL11 significantly inhibited CRC cell migration, invasion and EMT in vitro. In addition, down-regulation of CXCL11 reduced CRC cell growth and metastasis in vivo. Finally, we revealed that repression of CXCL11 inhibited the metastatic ability of CRC cell in a N-cadherin dependent manner.ConclusionIn summary, this study explicates the oncogenic activities of CXCL11 in CRC cell growth and metastasis.

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“…MUC12 and PRAC1 were similarly downregulated in both men and women when comparing RCCs to LCCs. Recent studies have examined mRNA expression using data from TCGA and GEO comparing patients with RCC to LCC have revealed similar changes to HOXC6, PRAC1 and MUC12 (Hu et al, 2018; Peng et al, 2018). The PRAC1 gene is associated with hypermethylation, and reported to be expressed in the prostate, rectum and left-sided colon.…”

Section: Discussionmentioning

confidence: 99%

“…Enrichment analysis, for example, evaluates high-dimensional data at the level of gene sets, and provides a large-scale comparison at the molecular pathway and disease process level instead of examining individual genes (Subramanian et al, 2005). In a recent paper, an enrichment analyses of gene expression correlation between RCC and LCC patients was carried out using the GSE14333 dataset from the public database National Center for Biotechnology Information Gene Expression Omnibus (GEO) (Peng et al, 2018). The study revealed molecular pathways that were differentially correlated with tumor development in these two regions of the colon.…”

Section: Introductionmentioning

confidence: 99%

“…The study revealed molecular pathways that were differentially correlated with tumor development in these two regions of the colon. However, in this study, only one population cohort was examined and did not correct for multiple comparison testing (Peng et al, 2018). Another study used data from both the Cancer Genome Atlas (TCGA) and GSE14333 to examine somatic mutations, genome-wide mRNA and miRNA, and DNA methylation profiles associated with RCC and found a correlation in the phosphoinositide 3-kinase (PI3K) signaling pathway (Hu et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

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Molecular pathway analysis indicates a distinct metabolic and immune phenotype in women with right-sided colon cancer

Sun

Mironova

Chen

et al. 2019

Preprint

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34Colon cancer is the third most commonly diagnosed cancer in the United States. Recent reports 35 have shown that the location of the primary tumor is of clinical importance. Patients with right-36 sided cancers (RCCs) (tumors arising between the cecum and proximal transverse colon) have 37 poorer clinical outcomes than those with left-sided colon cancers (LCCs) (tumors arising 38 between the distal transverse colon and sigmoid colon, excluding the rectum). Interestingly, 39 women have a lower incidence of colon cancer than men do. However, women have a higher 40 propensity for RCC than men. Identification of gene expression differences between RCC and 41 LCC is considered a potential means of prognostication. Furthermore, studying colon cancer 42 sidedness could reveal important predictive markers for response to various treatments. This 43 study provides a comprehensive bioinformatic analysis of various genes and molecular 44 pathways that correlated with sex and anatomical location of colon cancer using four publicly 45 available annotated datasets housed in the National Center for Biotechnology Information's 46 Gene Expression Omnibus (GEO). We identified differentially expressed genes in tumor 47 tissues from women with RCC, which showed attenuated energy and nutrient metabolism when 48 compared to women with LCC. Specifically, we showed that the downregulation of 5' AMP-49 activated protein kinase alpha subunit (AMPKα) and downregulated anti-tumor immune 50 response in women with RCC. This difference was not seen when comparing tumor tissues 51 from men with RCC to men with LCC. Therefore, women with RCC may have a specific 52 metabolic and immune phenotype which accounts for differences in prognosis and treatment 53 response. 54 55

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Identification of genomic expression differences between right-sided and left-sided colon cancer based on bioinformatics analysis

Cited by 14 publications

References 43 publications

Colorectal Cancer: Genetic Abnormalities, Tumor Progression, Tumor Heterogeneity, Clonal Evolution and Tumor-Initiating Cells

Colorectal Cancer: Genetic Abnormalities, Tumor Progression, Tumor Heterogeneity, Clonal Evolution and Tumor-Initiating Cells

Down-regulation of CXCL 11 inhibits colorectal cancer cell growth and epithelial-mesenchymal transition

Molecular pathway analysis indicates a distinct metabolic and immune phenotype in women with right-sided colon cancer

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