Objective: To investigate the expression patterns and underlying mechanisms of Lysyl Oxidase (LOX) in ovarian cancer, and to explore the correlation between its expression level and the clinical characteristics and therapeutic outcomes of the disease. Methods: The correlation between high LOX expression and the clinicopathological features, treatment outcomes，and prognosis of ovarian cancer was analyzed by the Cancer Genome Atlas (TCGA) .The expression characteristics of LOX mRNA in different ovarian cancer cells in the tumor microenvironment were explored by the TISCH2 database. The expression pattern of LOX in ovarian cancer tissues were confirmed through immunohistochemistry. Utilizing siRNA transfection technology to silence the expression and LOX, and then analyzing the differentially expressed genes between LOX-silencing and control fibroblasts through RNA sequencing, followed by Gene Set Enrichment Analysis (GSEA) to identify the signaling pathways that are differentially enriched between the LOX-silenced and control groups, with subsequent validation through Real-Time PCR. The effect of knocking down LOX in fibroblast on the sensitivity of ovarian cancer to paclitaxel was analyzed by determining the half-maximal inhibitory concentration (IC50). Furthermore, Western blot and Real-Time PCR were conducted to analyze the expression of LOX in human fibroblasts and mouse fibroblasts (L929) induced by paclitaxel. Results: High expression of LOX was significantly associated with the presence of tumors, poor treatment outcomes, and venous invasion in ovarian cancer. LOX was highly expressed in cancer associated fibroblasts in ovarian cancer. Silencing LOX led to the downregulation of cell adhesion molecule expression. Paclitaxel can induce upregulation of LOX expression in fibroblasts. Knocking down LOX in fibroblasts can increase the sensitivity of co-cultured fibroblasts and tumor cells to paclitaxel. Conclusion: High expression of LOX is associated with a poor prognosis in ovarian cancer, knocking down LOX in fibroblast can enhance the sensitivity of ovarian cancer to paclitaxel; the mechanism of LOX may linked to alterations in the expression of cell adhesion molecules in cancer-associated fibroblasts. Paclitaxel can upregulate the expression of LOX in fibroblasts.