Background: According to recent reports, some cancer subtypes have increased GAPLINC expression. The invasion and dissemination of cancer cells may be facilitated by GAPLINC expression. However, the therapeutic utility of GAPLINC in colon cancer (COAD) has not been studied. Materials/Methods: We evaluated the mRNA expression of GAPLINC in COAD patients using data from the Cancer Genome Map to identify the pathway connected with GAPLINC implicated in the etiology of COAD (TCGA). In this investigation, we used 480 tumor samples and 41 standard samples. Results: The expression of GAPLINC varied between normal and malignant samples, as seen by scatter plots and paired plots (P<0.05). An examination of overall survival time (OS) revealed that patients with COAD who had high GAPLINC expression had a poorer prognosis than patients with COAD who had low GAPLINC expression (P<0.05). GAPLINC expression and the main treatment result were independent prognostic factors for COAD patients in a multivariate Cox proportional hazards model research. According to GSEA findings, the reaction group's biological oxidation and angiogenesis pathways were too varied degrees enriched in the COAD samples with the GAPLINC overexpression phenotype. Genes relevant to the differentiation of epidermal cells and the control of endocrine processes were discovered in a GO investigation of individuals with high GAPLINC expression. The G protein-coupled receptor signal transduction pathway driven by phospholipase C was altered. Conclusions: Our findings support severe clinical characteristics associated with greater GAPLINC expression levels in COAD. A useful prognostic tool may be GAPLINC, a molecular biomarker linked to the poor prognosis of COAD patients.