Abstract
Simple SummaryThe diffuse-type of gastric cancer is associated with epithelial to mesenchymal transition. Loss of E-cadherin expression is the hallmark of this process and is largely due to the upregulation of the transcription factors ZEB1/2, Snail, Slug, and Twist1/2. However, miRNA and lncRNAs can also participate through these transcription factors which directly target E-cadherin. The competing endogenous RNA (ceRNA) network hypothesis state that lncRNA can sponge the miRNA pool that targets these transcripts. Based on the lack of said networks in the epithelial to mesenchymal transition, we performed a prediction analysis that resulted in novel ceRNA networks which will expand our knowledge of the molecular basis of the diffuse-type of gastric cancer.The diffuse-type of gastric cancer (DGC), molecularly associated with epithelial to mesenchymal transition (EMT), is increasing in incidence. Loss of E-cadherin expression is the hallmark of the EMT process and is largely due to the upregulation of the EMT-inducing transcription factors ZEB1/2, Snail, Slug, and Twist1/2. However, ncRNA, such as miRNA and lncRNAs, can also participate in the EMT process through the direct targeting of E-cadherin and other EMT-inducing transcription factors. Additionally, lncRNA can sponge the miRNA pool that targets these transcripts through competing endogenous RNA (ceRNA) networks. In this review, we focus on the role of ncRNA in the direct deregulation of E-cadherin, as well as EMT-inducing transcription factors. Based on the relevance of the ceRNA network hypothesis, and the lack of said networks in EMT, we performed a prediction analysis for all miRNAs and lncRNAs that target E-cadherin, as well as EMT-inducing transcription factors. This analysis resulted in novel predicted ceRNA networks for E-cadherin and EMT-inducing transcription factors (EMT-TFs), as well as the expansion of the molecular basis of the DGC.
Highlights
Gastric cancer (GC) is the fifth cause of incidence and the third-leading cause of cancer deaths worldwide [1]
A strong correlation with an characterization of a large set of clinical samples has defined this sub‐type of GC as genomically stable epithelial to mesenchymal transition (EMT) has been proposed by the Asian Cancer Research Group with low mutational burden, mostly restricted to the CDH1 (E‐cadherin) gene [20]
When are tumor cells reach metastatic and Twist1/2), knownand as EMT-inducing transcription factors (EMT-TF), frequently overexpressed sites, theyand perform the reverse process of EMT, known astumor a mesenchymal-epithelial transition (MET)
Summary
Gastric cancer (GC) is the fifth cause of incidence and the third-leading cause of cancer deaths worldwide [1]. The genetic architecture of the host and hereditary cancer susceptibility syndromes [7] (Figure 1) The former is preceded by clearly defined and sequentially ordered precancerous histological type (DGC). A strong correlation with an characterization of a large set of clinical samples has defined this sub‐type of GC as genomically stable epithelial to mesenchymal transition (EMT) has been proposed by the Asian Cancer Research Group with low mutational burden, mostly restricted to the CDH1 (E‐cadherin) gene [20]. A gene have been identified in familial clusters of GC, in hereditary diffuse gastric cancer recurrent loss of CDH1 expression is a common finding in this association. Mutations in the CDH1 gene have been identified in familial clusters of GC, in hereditary diffuse cancer (HDGC)ofsyndrome [22]
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