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Article Abstract
Background: Ovarian cancer (OC) is a leading cause of cancer deaths in women. Comprehensive molecular studies are required to understand OC pathogenesis. KRAS and NOXA genes are involved in tumorigenesis and disease progression. KRAS promotes tumor growth, while NOXA triggers the apoptotic signaling pathway.
Methods: Fifty-six ovarian cancer patients and twenty healthy controls were enrolled in the study. Gene expression profiling was performed utilizing the qRT-PCR assay. Then, the proteomic levels of KRAS and NOXA genes were assessed by the ELISA technique.
Results: The results showed that KRAS gene expression was significantly increased in OC patients compared to controls (p < 0.0001). Additionally, KRAS overexpression was correlated significantly with more aggressive characteristics, including advanced stage, positive lymph invasion, and metastatic status (p = 0.04, 0.05, and 0.02, respectively). In contrast, NOXA expression was downregulated in OC patients compared to controls (p = 0.001), and this reduction was more pronounced in patients with more aggressive characteristics (p = 0.001, 0.01, 0.0008, 0.02, respectively). At the transcriptomic level, KRAS concentration was higher among the patient group (p = 0.03) and correlated with aggressive tumor features (p = < 0.0001, 0.001, and 0.03, respectively). Interestingly, no significant changes were detected in NOXA protein levels concerning ovarian cancer development and progression. These findings were further confirmed by receiver operating characteristic (ROC) curve analysis, validating the genetic and transcriptomic results.
Conclusion: The differential expression of KRAS and NOXA genes holds promise as potential biomarkers for ovarian cancer development and progression. Specifically, KRAS transcriptomic levels serve as a reliable discriminator of ovarian cancer progression. In contrast, NOXA protein expression warrants further investigation to elucidate its role in the progression and pathophysiology of ovarian cancer.
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| http://dx.doi.org/10.1038/s41598-025-17650-6 | DOI Listing |
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12413452 | PMC |
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