A Comprehensive Review on the Importance of MiRNA-206 in the Animal Model and Human Diseases

Abstract

MicroRNA-206 (miR-206) is a microRNA that is involved in many human diseases, such as myasthenia gravis, osteoarthritis, depression, cancers, etc. Both inhibition effects and progression roles of miR-206 have been reported for the past few years. High expression of miR-206 was observed in patients with osteoarthritis, gastric cancer and epithelial ovarian cancer compared to normal people. The study also showed that miR-206 promotes cancer progression in breast cancer patients and avascular necrosis of the femoral head. Meanwhile, several studies have shown that expression levels of miR-206 were down-regulated in laryngeal carcinoma cell multiplication, as well as in hepatocellular carcinoma, non-small lung cancer and infantile hemangioma. Moreover, miR-206 was up-regulated in the mild stage of amyotrophic lateral sclerosis patients and then down-regulated in the moderate and severe stages, indicating that miR-206 has the double effects of starting and aggravating the disease. In neuropsychiatric disorders, such as depression, miR-206 also plays an important role in the progression of the disease; the level of miR-206 is most highly expressed in the brains of patients with depression. In the current review, we summarize the role of miR-206 in various diseases, and miR-206 may be developed as a new biomarker for diagnosing diseases in the near future.

Keywords: Alzheimer’s disease.; MiRNA; biomarkers; expression levels; human diseases; miR-206.

Fig. (1)

The canonical biogenesis of miR-206 is a complex pathway, which can be divided into two steps: nuclear and cytoplasmic steps. MiRNAs are derived from pri-miRNAs and processed into pre-miRNA with the help of Drosha. Finally, Dicer recognizes and splices it into a mature miRNA.

Fig. (2)

MiR-1, miR-206, miR-133a, and miR-133b take part in local skeletal muscle communication; the levels of serum miR-206 significantly increased after treatment with the therapeutic drug in skeletal muscle injury, and the action of miR-206 was linked by the upstream and downstream relationships.

Fig. (3)

The level of serum miR-206 was elevated in patients with mild cognition impairment (MCI) and promoted the AD symptom via inhibiting the level of BDNF in AD model brain tissue of mice.

Fig. (4)

Enhanced miR-206-3p levels and decreased BDNF expression were observed in both the hippocampus and mPFC of PS mice, and brain stereotactic injection of an antagomir of miR-206 increased BDNF expression and decreased stress-induced attack behavior in SI mice.

Fig. (5)

MiR-206 was dysregulated in HCC tissues of HCC patients and directly targeted G6PD and upregulated the expression of G6PD to promote hepatocellular carcinoma cell growth.

Fig. (6)

HMGB1 intramyocardial injection improved LV function and remodelling, and these effects were associated with miR-206 overexpression and miR-206-mediated inhibition of TIMP-3.

Fig. (7)

The expression level of miR-206 was decreased in lung cancer cells and negatively regulated CORO1C and then restrained the proliferation, migration and invasion of A549 cells. The level of miR-206 was noticeably decreased in advanced patients with gastric cancer compared to normal people. MiR-206 inhibited RCC cell growth partly by targeting GAK in RCC patients.