MicroRNAs: A novel potential biomarker for diagnosis and therapy in patients with non-small cell lung cancer

Abstract

Background: Lung cancer is still one of the most serious causes of cancer-related deaths all over the world. MicroRNAs (miRNAs) are defined as small non-coding RNAs which could play a pivotal role in post-transcriptional regulation of gene expression. Increasing evidence demonstrated dysregulation of miRNA expression associates with the development and progression of NSCLC.

Aims: To emphasize a variety of tissue-specific miRNAs, circulating miRNAs and miRNA-derived exosomes could be used as potential diagnostic and therapeutic biomarkers in NSCLC patients.

Materials & methods: In the current review, we paid attention to the significant discoveries of preclinical and clinical studies, which performed on tissue-specific miRNA, circulating miRNA and exosomal miRNA. The related studies were obtained through a systematic search of Pubmed, Web of Science, Embase.

Results: A variety of tissue-specific miRNAs and circulating miRNAs with high sensitivity and specificity which could be used as potential diagnostic and therapeutic biomarkers in NSCLC patients. In addition, we emphasize that the miRNA-derived exosomes become novel diagnostic biomarkers potentially in these patients with NSCLC.

Conclusion: MiRNAs have emerged as non-coding RNAs, which have potential to be candidates for the diagnosis and therapy of NSCLC.

Figure 1

Dysregulated miRNA participating in biological processes of lung cancer. The schematic representation depicting a variety of miRNA would emerge in cell proliferation, migration, invasion and apoptosis when down‐regulated or up‐regulated. It is known to us that miRNA play tumour suppressor and/or oncogenic roles in NSCLC by negatively modulating the target genes which exert tumour suppressor and/or oncogenic effect involved in cell proliferation, metastasis, invasion and apoptosis

Figure 2

miRNA involved in epithelial‐to‐mesenchymal transition (EMT) in NSCLC. The schematic representation depicting EMT is a pivotal process to promote tumour cells. miR‐134 inhibits EMT evidenced by up‐regulation of E‐cadherin expression and down‐regulation of vimentin and integrin subunit beta 1 (ITGB1) expression. miR‐206 inhibits EMT through decreased expression of c‐Met and Bcl2 in lung cancer cells. Slug is a potent trigger for EMT, and miR‐124 inhibits EMT by down‐regulating Slug protein. FHIT inhibits EMT through transcriptional repression of EMT‐related genes. A FHIT:Fragile histidine triad‐activated miRNA, miR‐30c, inhibits EMT via targeting metastasis‐related genes (MTDH) and high mobility group AThook 2 (HMGA2)