Objectives: Long non‐coding RNAs (lncRNAs) are a group of non‐protein‐coding RNAs that are greater than 200 nucleotides in length. Increasing evidence indicates that lncRNAs, which may serve as either oncogenes or tumour suppressor genes, play a vital role in the pathophysiology of human diseases, especially in tumourigenesis and progression. Deregulation of lncRNAs impacts different cellular processes, such as proliferation, dedifferentiation, migration, invasion and anti‐apoptosis. The aim of this review was to explore the molecular mechanism and clinical significance of long non‐coding RNA‐activated by transforming growth factor β (lncRNA‐ATB) in various types of cancers.Materials and methods: In this review, we summarize and analyze current studies concerning the biological functions and mechanisms of lncRNA‐ATB in tumour development. The related studies were obtained through a systematic search of Pubmed, Web of Science, Embase and Cochrane Library.Results: Long non‐coding RNAs‐ATB is a novel cancer‐related lncRNA that was recently found to exhibit aberrant expression in a variety of malignancies, including hepatocellular carcinoma, colorectal cancer, gastric cancer, and lung cancer. Dysregulation of lncRNA‐ATB has been shown to contribute to proliferation, migration and invasion of cancer cells. Long non‐coding RNAs‐ATB promotes tumourigenesis and progression mainly through competitively binding miRNAs to induce epithelial‐mesenchymal transition (EMT).Conclusions: Long non‐coding RNAs‐ATB likely represents a feasible cancer biomarker or therapeutic target.

Accumulating evidence has indicated that long non-coding RNAs (lncRNAs) behave as a novel class of transcription products during multiple cancer processes. However, the mechanisms responsible for their alteration in cholangiocarcinoma (CCA) are not fully understood. The expression of SPRY4-IT1 in CCA tissues and cell lines was determined by RT-qPCR, and the association between SPRY4-IT1 transcription and clinicopathologic features was analyzed. Luciferase reporter and chromatin immunoprecipitation (ChIP) assays were performed to explore whether SP1 could bind to the promoter region of SPRY4-IT1 and activate its transcription. The biological function of SPRY4-IT1 in CCA cells was evaluated both in vitro and in vivo. ChIP, RNA binding protein immunoprecipitation (RIP) and luciferase reporter assays were performed to determine the molecular mechanism of SPRY4-IT1 in cell proliferation, apoptosis and invasion. SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally, SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Furthermore, SPRY4-IT1 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion; inducing cell apoptosis and reversing the epithelial-to-mesenchymal transition (EMT) process in CCA cells. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold. Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p. Our data illustrate how SPRY4-IT1 plays an oncogenic role in CCA and may offer a potential therapeutic target for treating CCA.

Long non-coding RNAs (lncRNAs), which are a portion of non-protein-coding RNAs (ncRNAs), have manifested a paramount role in the pathophysiology of human diseases, particularly in pathogenesis and progression of disease. Myocardial infarction associated transcript (MIAT), which was recently found to demonstrate aberrant expression in various diseases, such as myocardial infarction, schizophrenia, ischemic stroke, diabetic complications, age-related cataract and cancers, is a novel disease-related lncRNA. This work summarize current evidence regarding the biological functions and underlying mechanisms of lncRNA MIAT during disease development. LncRNA MIAT likely represents a feasible cancer biomarker or therapeutic target.