The regulatory relationship between transcription factor STAT3 and noncoding RNA (ncRNA) is a critical area of research in cancer biology. STAT3, a key node in carcinogenic signaling pathways, is activated in various tumor tissues and plays important roles in tumor formation, metastasis, and drug resistance. Noncoding RNAs, including long noncoding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs), have been shown to be closely related to various epithelial-mesenchymal transition and drug resistance processes in tumor cells. This review aims to summarize the regulatory effects and mechanisms of STAT3 on lncRNAs, miRNAs, and circRNAs, as well as the regulation of STAT3 by ncRNAs. STAT3 can directly bind to the promoters of lncRNAs, upregulating their expression and subsequently affecting the biological phenotype and disease progression of cells. For example, STAT3 binds to the promoter of lncRNA *LINC00668*, upregulating its expression, which then promotes the proliferation, migration, and invasion of tumor cells by sponging miR-193a. Similarly, STAT3 binds to the promoter of lncRNA *TINCR*, enhancing its transcription, which upregulates the expression of *EGFR* by sponging miR-503-5p. Additionally, STAT3 can form positive feedback loops with lncRNAs and miRNAs, such as the STAT3/CASC9/miR-519d loop in gliomas and the STAT3/SNHG16/miR-503-5p loop in colorectal cancer. STAT3 can also affect miRNA expression by binding to miRNA promoters, promoting the occurrence and development of diseases. For instance, STAT3 binds to the promoter of miR-223 and miR-29a-5p, upregulating their expression, which then promotes tumor cell proliferation and invasion. However, STAT3 can also downregulate miRNA expression, forming negative feedback loops. For example, STAT3 inhibits the expression of miR-34a and miR-204, which can then enhance IL-6R activity and promote the invasion and migration of tumor cells. STAT3 can directly bind to the promoters of circRNAs, upregulating their expression and forming positive feedback loops. For example, circ-LRIG3 is upregulated in hepatocellular carcinoma (HCC) due to STAT3 binding to its promoter, which enhances STAT3 activity and promotes tumor cell proliferation and invasion. Additionally, circ-CCDC66 is upregulated in non-small cell lung cancer (NSCLC) due to STAT3 binding to its promoter, which promotes the proliferation, migration, and invasion of NSCLC cells by sponging miR-33The regulatory relationship between transcription factor STAT3 and noncoding RNA (ncRNA) is a critical area of research in cancer biology. STAT3, a key node in carcinogenic signaling pathways, is activated in various tumor tissues and plays important roles in tumor formation, metastasis, and drug resistance. Noncoding RNAs, including long noncoding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs), have been shown to be closely related to various epithelial-mesenchymal transition and drug resistance processes in tumor cells. This review aims to summarize the regulatory effects and mechanisms of STAT3 on lncRNAs, miRNAs, and circRNAs, as well as the regulation of STAT3 by ncRNAs. STAT3 can directly bind to the promoters of lncRNAs, upregulating their expression and subsequently affecting the biological phenotype and disease progression of cells. For example, STAT3 binds to the promoter of lncRNA *LINC00668*, upregulating its expression, which then promotes the proliferation, migration, and invasion of tumor cells by sponging miR-193a. Similarly, STAT3 binds to the promoter of lncRNA *TINCR*, enhancing its transcription, which upregulates the expression of *EGFR* by sponging miR-503-5p. Additionally, STAT3 can form positive feedback loops with lncRNAs and miRNAs, such as the STAT3/CASC9/miR-519d loop in gliomas and the STAT3/SNHG16/miR-503-5p loop in colorectal cancer. STAT3 can also affect miRNA expression by binding to miRNA promoters, promoting the occurrence and development of diseases. For instance, STAT3 binds to the promoter of miR-223 and miR-29a-5p, upregulating their expression, which then promotes tumor cell proliferation and invasion. However, STAT3 can also downregulate miRNA expression, forming negative feedback loops. For example, STAT3 inhibits the expression of miR-34a and miR-204, which can then enhance IL-6R activity and promote the invasion and migration of tumor cells. STAT3 can directly bind to the promoters of circRNAs, upregulating their expression and forming positive feedback loops. For example, circ-LRIG3 is upregulated in hepatocellular carcinoma (HCC) due to STAT3 binding to its promoter, which enhances STAT3 activity and promotes tumor cell proliferation and invasion. Additionally, circ-CCDC66 is upregulated in non-small cell lung cancer (NSCLC) due to STAT3 binding to its promoter, which promotes the proliferation, migration, and invasion of NSCLC cells by sponging miR-33