Long non-coding RNA (lncRNA) MIAT plays a significant role in hepatocellular carcinoma (HCC). MIAT is a well-known lncRNA that regulates carcinogenesis in various malignant tumors and is associated with poor prognosis. It is involved in the initiation of metastasis, invasion, cellular migration, and proliferation. MIAT is considered a potential theranostic agent and therapeutic target in several malignancies. The review highlights the molecular mechanisms of MIAT, including its downstream target genes, interactions with other ncRNAs, and potential clinical implications as a diagnostic and/or prognostic biomarker in HCC. MIAT is located on chromosome 22q12.1 and is transcribed from the sense strand of the genome. It has multiple single nucleotide polymorphisms (SNPs) associated with increased susceptibility to myocardial infarction. MIAT is involved in various physiological processes, including cardiovascular diseases and solid malignancies such as HCC, breast cancer, and lung cancer. It acts as a sponge for miRNAs, altering downstream signaling pathways that regulate cellular proliferation, apoptosis, and inflammation. In HCC, MIAT promotes tumor growth and progression by increasing proliferation, invasion, and migration. It interacts with miRNAs such as miR-214-3p and miR-520d-3p, which are involved in cell cycle regulation and proliferation. MIAT also contributes to HCC chemoresistance and immune escape by modulating the expression of PD-L1, a key player in immune checkpoint signaling. MIAT has potential clinical applications as a diagnostic biomarker and therapeutic target in HCC. Its expression levels may serve as an early indicator of cancer and could be used to predict treatment response. Inhibiting MIAT expression may be an effective way to treat HCC, and targeted therapies such as small interfering RNAs (siRNAs) or antisense oligonucleotides (ASOs) could be used to achieve this. While the role of MIAT in HCC is becoming increasingly apparent, there are limitations in current research, including the lack of human trials and the need for further investigation into its complex regulatory mechanisms. Future studies should focus on elucidating the detailed mechanisms by which MIAT regulates HCC progression and exploring its potential as a diagnostic marker or therapeutic target. Additionally, the systemic influence of MIAT on other diseases such as myocardial infarction and diabetic retinopathy could provide valuable insights and enhance its clinical relevance.Long non-coding RNA (lncRNA) MIAT plays a significant role in hepatocellular carcinoma (HCC). MIAT is a well-known lncRNA that regulates carcinogenesis in various malignant tumors and is associated with poor prognosis. It is involved in the initiation of metastasis, invasion, cellular migration, and proliferation. MIAT is considered a potential theranostic agent and therapeutic target in several malignancies. The review highlights the molecular mechanisms of MIAT, including its downstream target genes, interactions with other ncRNAs, and potential clinical implications as a diagnostic and/or prognostic biomarker in HCC. MIAT is located on chromosome 22q12.1 and is transcribed from the sense strand of the genome. It has multiple single nucleotide polymorphisms (SNPs) associated with increased susceptibility to myocardial infarction. MIAT is involved in various physiological processes, including cardiovascular diseases and solid malignancies such as HCC, breast cancer, and lung cancer. It acts as a sponge for miRNAs, altering downstream signaling pathways that regulate cellular proliferation, apoptosis, and inflammation. In HCC, MIAT promotes tumor growth and progression by increasing proliferation, invasion, and migration. It interacts with miRNAs such as miR-214-3p and miR-520d-3p, which are involved in cell cycle regulation and proliferation. MIAT also contributes to HCC chemoresistance and immune escape by modulating the expression of PD-L1, a key player in immune checkpoint signaling. MIAT has potential clinical applications as a diagnostic biomarker and therapeutic target in HCC. Its expression levels may serve as an early indicator of cancer and could be used to predict treatment response. Inhibiting MIAT expression may be an effective way to treat HCC, and targeted therapies such as small interfering RNAs (siRNAs) or antisense oligonucleotides (ASOs) could be used to achieve this. While the role of MIAT in HCC is becoming increasingly apparent, there are limitations in current research, including the lack of human trials and the need for further investigation into its complex regulatory mechanisms. Future studies should focus on elucidating the detailed mechanisms by which MIAT regulates HCC progression and exploring its potential as a diagnostic marker or therapeutic target. Additionally, the systemic influence of MIAT on other diseases such as myocardial infarction and diabetic retinopathy could provide valuable insights and enhance its clinical relevance.