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MicroRNAs (miRNAs) are small non-coding RNA molecules, approximately 22 nucleotides in length that regulate gene translation through silencing or degradation of target mRNAs. They are involved in multiple biological processes, including differentiation and proliferation, metabolism, hemostasis, apoptosis or inflammation, and in the pathophysiology of many diseases. Numerous studies have suggested circulating miRNAs as promising diagnostic and prognostic biomarkers of many diseases.

MiR-140 is encoded within intron 16 of Wwp2, an E3 ubiquitin ligase. It was first identified as a key player in cartilage development and homeostasis in chondrocytes. The regulation of miR-140 was reported to be tissue-dependent. Besides its role in chondrocytes, it was found to be expressed in numerous other tissues and cell types including brain, breast, lung, colon, ovary and testis.

Importantly, expression-profiling experiments revealed a potential tumor suppressor function for miR-140 in many cancers where its expression was found to be downregulated in cutaneous squamous cell carcinoma, basal cell carcinoma, osteosarcoma, breast cancer, ovarian cancer, bladder cancer, gastric cancer, colon cancer and lung squamous cell carcinoma. Inversely, it was revealed a correlation between miR 140-3p overexpression with chordoma invasion and recurrence suggesting poor prognosis of spinal chordoma. miR-140 also has been demonstrated to be associated with progression of many conditions including renal cell carcinoma or osteoarthritis. In addition, miR 140-3p is found to be ectopic and implicated in proliferation, migration and invasion in NSCLC cells. It was reported that the level of plasma exosomal miR 140-3p in colorectal cancer (CRC) patients was lower than that in healthy controls. The decreased miR-140-3p level was also observed in CRC patients with liver metastasis. The expression of miR 140-3p in CRC tissues were significantly lower than that in matched normal tissues. Functionally, miR 140-3p overexpression suppressed proliferation, migration, invasion, and β-catenin nuclear translocation, as well as promoted apoptosis in LoVo cells, while inhibition of miR-140-3p reversed these cellular processes in HCT 116 cells.

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