MicroRNAs modulation in lung cancer: exploring dual mechanisms and clinical prospects

The global incidence of lung cancer is marked by a considerably elevated mortality rate. MicroRNAs (miRNAs) exert pivotal influence in the intricate orchestration of gene regulation, and their dysregulation can precipitate dire consequences, notably cancer. Within this context, miRNAs encapsulated in exosomes manifest a diversified impact on the landscape of lung cancer, wherein their actions may either foster angiogenesis, cell proliferation, and metastasis, or counteract these processes. This comprehensive review article discerns potential targets for the prospective development of therapeutic agents tailored for lung cancer. Tumor-suppressive miRNAs, such as miR204, miR-192, miR-30a, miR-34a, miR-34b, miR-203, and miR-212, exhibit heightened expression and demonstrate the capacity to inhibit cellular proliferation and invasiveness. Conversely, the deleterious effects of tumor-promoting miRNAs like miR-21, miR-106a, miR-155, miR-205, and miR-210 can be attenuated through the application of their respective inhibitors. Distinct miRNAs selectively target various oncogenes, including NUAK Family Kinase 1 Proliferation and apoptosis adaptor protein 15 (PEA-15/PED), Hypoxia-inducible factor 1-alpha (HIF1), as well as tumor suppressor genes such as phosphatase and tensin homolog (PTEN), Suppressor of cytokine signaling 1 (SOCS1), Tumor protein P53 binding protein 1 (TP53BP1), and PH Domain and Leucine Rich Repeat Protein Phosphatase 2 (PHLP22). This investigative approach proves invaluable in elucidating the specific miRNAs implicated in the deregulation of crucial genes pivotal to the pathogenesis of cancer.