Abstract
(1) Background: Lysyl oxidase (LOX) plays a dual role in carcinogenesis and studies show a higher risk of cancer in LOX G473A variants. The present study evaluated the pattern of LOX G473A polymorphism (rs1800449) and serum LOX levels in ovarian cancer patients. (2) Methods: Serum LOX levels were estimated by enzyme linked immunosorbent assay (ELISA). A polymorphism of rs1800449 of LOX gene was detected by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Selected samples were sequenced for external validation. (3) Results: A majority of study participants were from low socio-economic status. Serum LOX level was significantly higher in ovarian cancer patients as compared to control. Serum LOX level in early-stage ovarian cancer was significantly lower as compared to advanced stage (FIGO stage III & IV). Wild type GG genotype was used as reference. Genotypes AA were associated with a significant risk of epithelial ovarian cancer (OR 3.208; p value- 0.033). A allele of rs1800449 polymorphism of LOX gene, the odds ratio was 1.866 (95% Confidence Interval 1.112–3.16) p value = 0.017 (4) Conclusions: A allele of rs1800449 polymorphism of LOX gene presents an increased risk of ovarian cancer in East Indian population. Serum LOX levels could be a potential biomarker for the diagnosis and prognosis of ovarian cancer.
Highlights
Ovarian cancer is one of the most commonly occurring cancers in women, the eighth most commonly occurring cancer worldwide, with 313,959 reported new cases and 207,252 deaths [1]
Wang et al reported Lysyl oxidase (LOX) G473A polymorphism as a risk factor for ovarian cancer, but they did not find significant difference in the frequency of the LOX G473A polymorphism when they categorized the patients based on tumor histology or tumor grade [37]
The frequency of the LOX G473A polymorphism, the AA genotype was found significantly higher in ovarian cancer patients as compared to control subjects
Summary
Ovarian cancer is one of the most commonly occurring cancers in women, the eighth most commonly occurring cancer worldwide, with 313,959 reported new cases and 207,252 deaths [1]. 5–10% of ovarian cancer cases develop due to a genetic predisposition [5,6]. Despite extensive studies on genetic alterations in ovarian cancer, the complexity of this disease precludes understanding of its aetiopathogenesis [7]. The tumor microenvironment comprises of cellular components like fibroblasts, immune cells, and endothelial cells. Non-cellular components such as the extracellular matrix (ECM), ECM remodeling enzymes, e.g., matrix metalloproteinase (MMPs), tissue inhibitors of metalloproteinase (TIMPs), Lysyl oxidases (LOXs), and growth factors (e.g., vascular endothelial growth factor, transforming growth factor beta, and platelet derived growth factor) play a major role in abnormal growth, local invasion, and metastasis, thereby promoting cancer progression [8,9,10,11,12]
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