MicroRNAs (miRNAs) are small non-coding RNA molecules that regulate gene expression and have been implicated in various biological processes, including cancer development and progression. This review discusses the role of miRNAs in cancer, their potential as diagnostic, prognostic, and therapeutic tools, and their involvement in tumor biology. MiRNAs are expressed in a wide range of organisms and are highly conserved. They are processed from primary transcripts by enzymes Drosha and Dicer, resulting in mature miRNAs that can regulate gene expression by binding to the 3'UTR of target mRNAs. Aberrant miRNA expression is a hallmark of cancer, and miRNAs can function as oncogenes or oncosuppressors depending on the cellular context and their target genes. In chronic lymphocytic leukemia (CLL), miR-15a and miR-16-1 are located at 13q14 and are frequently deleted, leading to loss of these miRNAs and contributing to the pathogenesis of CLL. miR-15a and miR-16-1 target BCL2, an oncogene involved in cell survival, and their loss leads to increased BCL2 expression and tumor development. Other miRNAs, such as miR-155 and miR-29, are also involved in cancer progression, with miR-155 promoting tumor growth and miR-29 suppressing tumor growth by targeting oncogenes like MCL1. In solid tumors, miRNAs such as miR-21 are overexpressed and contribute to tumor progression by regulating cell survival and proliferation. miR-21 also targets tumor suppressor genes like PTEN and PDCD4. Conversely, miR-125b and miR-205 are downregulated in some cancers and regulate oncogenes like HER-2 and HER-3. MiRNAs are also involved in invasion, angiogenesis, and metastasis. For example, miR-10b promotes metastasis by inhibiting the translation of HOXD10 and increasing RHOC expression. miR-373 and miR-520c promote tumor invasion and metastasis. MiR-21 stimulates invasion, extravasation, and metastasis in various cancers, while miR-205 reduces invasion and suppresses lung metastasis. MiRNAs can also influence epigenetic regulation, with miR-29 targeting DNA methyltransferases and reactivating tumor suppressor genes. Epigenetic changes, such as DNA methylation, can alter miRNA expression, contributing to cancer development. The use of epigenetic drugs, such as DNA demethylating agents and histone deacetylase inhibitors, can restore miRNA expression and potentially reverse tumoral phenotypes. In cancer treatment, miRNAsMicroRNAs (miRNAs) are small non-coding RNA molecules that regulate gene expression and have been implicated in various biological processes, including cancer development and progression. This review discusses the role of miRNAs in cancer, their potential as diagnostic, prognostic, and therapeutic tools, and their involvement in tumor biology. MiRNAs are expressed in a wide range of organisms and are highly conserved. They are processed from primary transcripts by enzymes Drosha and Dicer, resulting in mature miRNAs that can regulate gene expression by binding to the 3'UTR of target mRNAs. Aberrant miRNA expression is a hallmark of cancer, and miRNAs can function as oncogenes or oncosuppressors depending on the cellular context and their target genes. In chronic lymphocytic leukemia (CLL), miR-15a and miR-16-1 are located at 13q14 and are frequently deleted, leading to loss of these miRNAs and contributing to the pathogenesis of CLL. miR-15a and miR-16-1 target BCL2, an oncogene involved in cell survival, and their loss leads to increased BCL2 expression and tumor development. Other miRNAs, such as miR-155 and miR-29, are also involved in cancer progression, with miR-155 promoting tumor growth and miR-29 suppressing tumor growth by targeting oncogenes like MCL1. In solid tumors, miRNAs such as miR-21 are overexpressed and contribute to tumor progression by regulating cell survival and proliferation. miR-21 also targets tumor suppressor genes like PTEN and PDCD4. Conversely, miR-125b and miR-205 are downregulated in some cancers and regulate oncogenes like HER-2 and HER-3. MiRNAs are also involved in invasion, angiogenesis, and metastasis. For example, miR-10b promotes metastasis by inhibiting the translation of HOXD10 and increasing RHOC expression. miR-373 and miR-520c promote tumor invasion and metastasis. MiR-21 stimulates invasion, extravasation, and metastasis in various cancers, while miR-205 reduces invasion and suppresses lung metastasis. MiRNAs can also influence epigenetic regulation, with miR-29 targeting DNA methyltransferases and reactivating tumor suppressor genes. Epigenetic changes, such as DNA methylation, can alter miRNA expression, contributing to cancer development. The use of epigenetic drugs, such as DNA demethylating agents and histone deacetylase inhibitors, can restore miRNA expression and potentially reverse tumoral phenotypes. In cancer treatment, miRNAs