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The **Septin 9 gene** encodes a cytoskeletal GTPase involved in cell division, chromosome segregation, and maintaining genomic stability. In a healthy state, the gene helps prevent tumor formation through normal cellular functions including cytokinesis and autophagy[3]. In several cancers, particularly **colorectal cancer (CRC)**, the *SEPT9* gene promoter region becomes hypermethylated. This methylation represses gene expression, disabling its tumor-suppressive roles and contributing to malignant transformation and progression[3][4]. The detection of methylated SEPT9 DNA in plasma is highly specific for CRC, and is FDA-approved as a non-invasive, blood-based biomarker for CRC screening (notably the Epi proColon assay). It is not a classical therapeutic target but is widely used as a **diagnostic and monitoring biomarker** for CRC and as a prognostic marker in other cancers such as hepatocellular carcinoma[5][7]. There are no known direct drug interactions or targeted therapies acting on the methylation status of the SEPT9 gene, and its clinical relevance is as a biomarker rather than a molecular drug target. Note: The “target” in this query is a methylation status (an epigenetic biomarker), not a biological molecule directly targetable by drugs. Thus, it is not a therapeutic target in the traditional sense; instead, it is a clinically validated **biomarker** for colorectal cancer diagnosis, prognosis, and monitoring[3][4][5][6].
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