New therapeutic axis in blood malignancies involving microRNAs and JAK/STAT3 signaling
AbstractCancers of the blood stemming from genetic or environmental abnormalities are included in the broad category of blood diseases. Some forms of leukemia may respond better to therapy than others, and there are a number of factors that contribute to the failure of current medications to effectively address blood diseases, including drug resistance. Many different factors, both inherited and acquired, may cause leukemia, which is characterized by the uncontrolled growth of one or more cell lines. Oncogene signal transducer and activator of transcription (STAT) family transcription factor STAT3, in particular, plays a crucial role in the initiation and development of hematological illnesses as a result of mutations, malfunction, or hyperactivity. In addition, research indicates that microRNAs, as biological molecules, may promote or inhibit tumor growth in different types of cancer. Additionally, it has been found that STAT3 has a robust connection to miRNA. For example, miRNAs may control STAT3 by targeting its upstream mediators such as IL6, IL9, and JAKs or directly binding to the STAT3 gene. However, STAT3 has the ability to control miRNAs. The purpose of this review was to identify the function of microRNAs and STAT3 and how they interact with one another in hematological malignancies.