MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression and play critical roles in human cancer. Dysregulation of miRNA expression is a common feature in cancer, occurring through mechanisms such as gene amplification or deletion, abnormal transcriptional control, epigenetic changes, and defects in miRNA biogenesis. MiRNAs can function as either oncogenes or tumor suppressors, influencing key cancer hallmarks such as sustaining proliferative signaling, evading growth suppressors, resisting cell death, activating invasion and metastasis, and inducing angiogenesis. They are also potential biomarkers for cancer diagnosis, prognosis, and treatment. MiRNA biogenesis involves transcription, processing by Drosha and Dicer, and incorporation into the RNA-induced silencing complex (RISC). MiRNAs regulate gene expression by binding to target mRNAs, either through imperfect or perfect complementarity, leading to translational repression or mRNA degradation. Additionally, miRNAs can act as ligands to activate signaling pathways, such as Toll-like receptor signaling, which can promote metastasis. Dysregulation of miRNA expression in cancer can occur through various mechanisms, including chromosomal abnormalities, transcriptional control changes, and defects in the miRNA biogenesis machinery. For example, miR-15a and miR-16-1 are frequently deleted in chronic lymphocytic leukemia and act as tumor suppressors by inducing apoptosis. Other miRNAs, such as miR-17-92, are overexpressed in various cancers and can promote cell proliferation. MiRNAs also regulate cell proliferation by targeting cell-cycle components and signaling pathways. They can influence cell survival by modulating anti-apoptotic and pro-apoptotic factors. MiRNAs are involved in resisting cell death by targeting Bcl-2 and Bcl-xL, and by regulating the extrinsic apoptotic pathway. MiRNAs play a significant role in activating invasion and metastasis by regulating epithelial-mesenchymal transition (EMT) and promoting cell migration and invasion. They are also involved in inducing angiogenesis by regulating hypoxia-inducible factor (HIF) and vascular endothelial growth factor (VEGF) signaling pathways. The dysregulation of miRNAs in cancer is a complex process, and further research is needed to identify their critical targets and establish their role in malignant transformation. MiRNAs have the potential to serve as diagnostic biomarkers, prognostic indicators, and therapeutic targets for cancer treatment. However, challenges remain in validating their clinical applications and developing efficient delivery systems for miRNA-based therapies.MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression and play critical roles in human cancer. Dysregulation of miRNA expression is a common feature in cancer, occurring through mechanisms such as gene amplification or deletion, abnormal transcriptional control, epigenetic changes, and defects in miRNA biogenesis. MiRNAs can function as either oncogenes or tumor suppressors, influencing key cancer hallmarks such as sustaining proliferative signaling, evading growth suppressors, resisting cell death, activating invasion and metastasis, and inducing angiogenesis. They are also potential biomarkers for cancer diagnosis, prognosis, and treatment. MiRNA biogenesis involves transcription, processing by Drosha and Dicer, and incorporation into the RNA-induced silencing complex (RISC). MiRNAs regulate gene expression by binding to target mRNAs, either through imperfect or perfect complementarity, leading to translational repression or mRNA degradation. Additionally, miRNAs can act as ligands to activate signaling pathways, such as Toll-like receptor signaling, which can promote metastasis. Dysregulation of miRNA expression in cancer can occur through various mechanisms, including chromosomal abnormalities, transcriptional control changes, and defects in the miRNA biogenesis machinery. For example, miR-15a and miR-16-1 are frequently deleted in chronic lymphocytic leukemia and act as tumor suppressors by inducing apoptosis. Other miRNAs, such as miR-17-92, are overexpressed in various cancers and can promote cell proliferation. MiRNAs also regulate cell proliferation by targeting cell-cycle components and signaling pathways. They can influence cell survival by modulating anti-apoptotic and pro-apoptotic factors. MiRNAs are involved in resisting cell death by targeting Bcl-2 and Bcl-xL, and by regulating the extrinsic apoptotic pathway. MiRNAs play a significant role in activating invasion and metastasis by regulating epithelial-mesenchymal transition (EMT) and promoting cell migration and invasion. They are also involved in inducing angiogenesis by regulating hypoxia-inducible factor (HIF) and vascular endothelial growth factor (VEGF) signaling pathways. The dysregulation of miRNAs in cancer is a complex process, and further research is needed to identify their critical targets and establish their role in malignant transformation. MiRNAs have the potential to serve as diagnostic biomarkers, prognostic indicators, and therapeutic targets for cancer treatment. However, challenges remain in validating their clinical applications and developing efficient delivery systems for miRNA-based therapies.