Fig. 2

miR-155 participates in multiple cellular functions. It is possible that hypoxic circumstances might lead to an increase in the production of miR-155 in cancer cells. This is because some response elements are present in the promoter region of miR-155. This particular microRNA has a strong connection to inflammation and exerts a major impact on lung cancer, ultimately having the capacity to alter the survival of cancer cells. In order to accomplish this objective, the levels of the tumor suppressor protein VHL are decreased, which in turn stimulates the development of new blood vessels. One-way TGF facilitates metastasis is by increasing miR-155 levels. This is accomplished through the action of Smad4. MiR-155 reduces RhoA protein levels, which breaks tight junctions and improves epithelial cell plasticity. This results in enhanced invasiveness and migration via enhancing epithelial–mesenchymal transition (EMT), which is triggered by transforming growth factor-beta 3. It is possible that lowering or inhibiting miR-155 could cause cells to halt in the G0/G1 phase of the cell cycle, which will signal the beginning of the process of programmed cell death. As a consequence of this, the growth of cancer cells in DLBCL and ccRC is restricted thanks to this. Another study showed that miR-155 inhibits Caspase 3 activity, which results in reduced cell death in nasopharyngeal cancer. Additionally, miR-155 has the potential to impact glucose metabolism by improving insulin sensitivity. This happens as a result of the suppression of C/EBPβ, which is a negative regulator in the insulin signaling pathway. This, in turn, leads to an increase in glycolysis. Ultimately, the presence of miR-155 is related with lowered levels of SOCS1 in non-small cell lung cancer (NSCLC), which might ultimately contribute to worse survival rates