This review outlines the activities of mirR99 family members in different cancers. Though the functional roles of these miRs are well described in some malignancies, the functional functions of these family members in other forms of cancer remain uncertain. The development and use of engineered mouse models such as miR99a KO, miR100 KO, or miR99a/100 DKO mice challenged with the type or subtype of the cancer in question would be extremely beneficial in determining the physiological and pathological roles of members of this family in different types of cancer and immune cell subtypes.The miR99 family members, which include miR99a, miR99b, and miR100, are key components of a regulatory network that governs several aspects of the cell life cycle, including differentiation, metabolism, survival and death. They are involved in the deregulation of numerous critical pathways including growth factor receptors like FGFR and IGF1R, Notch, mTOR, TGFB and Wnt signaling pathways to alter cellular function. In addition, the typical miR99 target, mTOR, appears to be at the core of the regulatory network miR99, and is more commonly involved in miR99-mediated dysregulation of cell activity. Given the importance of mTOR signaling in a number of illnesses, it looks suitable to use miR99 family members as a therapeutic intervention to deal with these illnesses. mTOR depletion did not result in upregulating miR99a in OSCC cells. In addition, an aberrant activation of PI3K/AKT/mTOR signaling in AMLs, despite increased expression of miR99 family members in AMLs. All in all, this evidence alludes to the existence of an unknown mechanism that maintains mTOR activity running despite the presence in these cells of a high level of miR99 family members. Modulation of miR99 activity might be a viable method for changing the expression of Treg in autoimmune diseases.
mHealth Hope or Hype : Experiences from Cell-Life