MicroRNAs and Synaptic Plasticity: From Their Molecular Roles to Response to Therapy.

Synaptic plasticity is the ability of synapses to weaken or strengthen over time, in response to changes in the activity of the neurons. It is orchestrated by a variety of genes, proteins, and external and internal factors, especially epigenetic factors. MicroRNAs (miRNAs) are well-acknowledged epigenetic modulators that regulate the translation and degradation of target genes in the nervous system. Increasing evidence has suggested that a number of miRNAs play important roles in modulating various aspects of synaptic plasticity. The deregulation of miRNAs could be associated with pathological alterations in synaptic plasticity, which could lead to different CNS-related diseases. Herein, we provide an update on the role of miRNAs in governing synaptic plasticity. In addition, we also summarize recent researches on the role of miRNAs in drug addiction, and their targets and mechanism of action. Understanding of the way in which miRNAs contribute to synaptic plasticity provides rational clues in establishing the novel biomarkers and new therapeutic strategies for the diagnosis and treatment of plasticity-related diseases and drug addiction.

Interplays between non-coding RNAs and chemokines in digestive system cancers.

Within tumors, chemokines and their cognate receptors are expressed by infiltrated leukocytes, cancerous cells, and related cells of stroma, like tumor-associated fibroblasts and tumor-associated macrophages. In malignancies, the altered expression of chemokines/chemokine receptors governs leukocyte infiltration and activation, epithelial-mesenchymal transition (EMT), cancer cell proliferation, angiogenesis, and metastasis. Non-coding RNAs (ncRNAs) contribute to multiple physiological and pathophysiological processes. Some miRNAs can exert anti-tumorigenic activity in digestive system malignancies by repressing the expression of tumor-promoting chemokines/chemokine receptors or by upregulating tumor-suppressing chemokines/chemokine receptors. However, many miRNAs exert pro-tumorigenic activity by suppressing the expression of chemokines/chemokine receptors or by upregulating tumor-promoting chemokines/chemokine receptors. LncRNA and circRNAs also exert pro- and anti-tumorigenic effects by targeting downstream miRNAs influencing the expression of tumor-promoting and tumor-suppressor chemokines/chemokine receptors. On the other side, some chemokines influence the expression of ncRNAs affecting tumor formation. The current review explains the communications between ncRNAs and chemokines/chemokine receptors in certain digestive system malignancies, such as gastric, colorectal, and pancreatic cancers and hepatocellular carcinoma to gain better insights into their basic crosstalk as well as possible therapeutic modalities.