Abstract
Esophageal cancer (EC) and gastric cancer (GC) often have an unfavorable prognosis. Therefore, research is being conducted to identify the molecular mechanisms underlying the tumorigenesis and progression of GC and EC, and to indicate novel therapeutic targets and clinically applicable biomarkers. The dysregulations and roles of long non-coding RNAs (lncRNAs) have been widely reported, and current published literature has shown that lncRNAs play important regulatory roles in the carcinogenesis and progression of EC and GC. The lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been investigated in a number of studies with regard to its pathogenic pathways and association with the prognosis of gastric and esophageal malignancies. As literature on the topic of MALAT1 in EC and GC continues to emerge, the present review aims to summarize all current knowledge on the association between MALAT1 expression and esophagogastric malignancies and to describe the pathogenic pathways and possible prognostic role of MALAT1 in esophagogastric cancer. As research studies on MALAT1 pathways in esophagogastric malignancies are ongoing, new possibilities for the diagnosis, prognosis and therapy of GC and EC are likely to be identified.
Highlights
Esophageal cancer (EC) and gastric cancer (GC) often have an unfavorable prognosis
The expression of long non‐coding RNAs (lncRNAs) can be inhibited by miRNAs through an argonaute 2‐medi‐ ated pathway. miR‐101 and miR‐217 have been demonstrated to act as tumor suppressor genes by targeting metastasis‐associated lung adeno‐ carcinoma transcript 1 (MALAT1) during esophageal squamous cell carcinoma (ESCC) development [8]
There is evidence to suggest that the posttranscriptional silencing of MALAT1 by miR‐101 and miR‐217 occurs in ESCC cells, which may significantly suppress the proliferation of the cells via G2/M cell cycle arrest
Summary
In patients with ESCC, MALAT‐1 is expressed at higher levels in cancer tissues compared with paired adjacent normal tissues, and in ESCC cell lines, MALAT‐1 knockdown reduces proliferation, increases apoptosis, inhibits migration, invasion and colony formation, and leads to cell cycle arrest at the G2/M phase [6]. There is evidence to suggest that the posttranscriptional silencing of MALAT1 by miR‐101 and miR‐217 occurs in ESCC cells, which may significantly suppress the proliferation of the cells via G2/M cell cycle arrest This may be due to suppression of the MALAT1‐mediated upregulation of p21 and p27 expression and inhibition of B‐MYB expression. It has been shown that the silencing of MALAT1 downregulates the expression of OCT4 and NANOG genes, which inhibits EC cell proliferation, migration and tumor sphere formation, while increasing cell apoptosis. MALAT1, inhibit the migration healthy tissues) and invasion of ESCC cells and induce G2/M phase arrest. New possibilities for the diagnosis, prognosis and treatment of patients with esopha‐ geal adenocarcinoma may emerge in future studies
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