Antiviral Peptides Derived from Plants: Their Designs and Functions.

In recent years, plant-derived bioactive compounds have been developed as antiviral agents. Plants synthesize a variety of compounds, especially peptides, which possess antimicrobial activity. Current studies have shown that some antimicrobial peptides have antiviral activity against a wide range of human DNA and RNA viruses and play an effective role in the treatment of human viral diseases. These peptides act through different mechanisms. They can integrate into the envelope of the target virus or cell membrane of the host, resulting in an unstable membrane. For instance, some peptides prevent the attachment of viral spike proteins to host cells. On the other hand, some peptides may alter the cellular pathways, including DNA replication or protein synthesis, leading to the suppression of viral infection. However, the antiviral activity of peptides can be affected by their chemical and structural properties. In several studies, the properties of antimicrobial (antiviral) peptides were altered by minor modifications, but these changes require tools to predict. Recently, computational approaches have been introduced to analyze the effects of structural modifications on the physicochemical properties, mechanism of action, stability, and activity of peptides. In this mini-review, we will describe the design and function of antiviral peptides derived from plants.

STAT3-EMT axis in tumors: Modulation of cancer metastasis, stemness and therapy response.

Epithelial-to-mesenchymal transition (EMT) mechanism is responsible for metastasis of tumor cells and their spread to various organs and tissues of body, providing undesirable prognosis. In addition to migration, EMT increases stemness and mediates therapy resistance. Hence, pathways involved in EMT regulation should be highlighted. STAT3 is an oncogenic pathway that can elevate growth rate and migratory ability of cancer cells and induce drug resistance. The inhibition of STAT3 signaling impairs cancer progression and promotes chemotherapy-mediated cell death. Present review focuses on STAT3 and EMT interaction in modulating cancer migration. First of all, STAT3 is an upstream mediator of EMT and is able to induce EMT-mediated metastasis in brain tumors, thoracic cancers and gastrointestinal cancers. Therefore, STAT3 inhibition significantly suppresses cancer metastasis and improves prognosis of patients. EMT regulators such as ZEB1/2 proteins, TGF-ß, Twist, Snail and Slug are affected by STAT3 signaling to stimulate cancer migration and invasion. Different molecular pathways such as miRNAs, lncRNAs and circRNAs modulate STAT3/EMT axis. Furthermore, we discuss how STAT3 and EMT interaction affects therapy response of cancer cells. Finally, we demonstrate targeting STAT3/EMT axis by anti-tumor agents and clinical application of this axis for improving patient prognosis.