Study the Impact of NADPH oxidase1,TNF-alpha and Cyclooxygenase-2 On Colon Cancer Patients.

BACKGROUND

Colon cancer is a major health concern globally, being one of the most commonly diagnosed cancers. Inflammation and oxidative stress are critical factors contributing to its development and progression. Understanding the roles of key molecules such as NOX1, TNF-α, and COX-2 in these processes may provide insights into potential biomarkers for early detection and targeted therapy.

OBJECTIVE

This study aims to investigate the roles of NADPH oxidase 1 (NOX1), Tumor Necrosis Factor-alpha (TNF-α), and Cyclooxygenase-2 (COX-2) in colon cancer progression and their possible implications in the disease context.

METHODS

A comparative analysis was conducted involving 40 colon cancer patients (15 males, 25 females; aged 20-78 years) and 40 healthy controls (17 males, 23 females; aged 21-75 years). Blood samples were collected from participants between October 10, 2023, and February 18, 2024. The levels of NOX1, TNF-α, and COX-2 were measured using the enzyme-linked immunosorbent assay (ELISA) method.

RESULTS

The study found significantly elevated levels of TNF-α in colon cancer patients (100.9-454.3 ng/L) compared to healthy controls (24.85-216.9 ng/L). Additionally, COX-2 levels were markedly higher in patients (239.4-690.53 units/L) than in controls (23.78-115.5 units/L). NOX1 levels were also elevated in cancer patients (4.0-14.92) relative to healthy subjects (0.89-9.39). These findings suggest an association between increased levels of TNF-α, COX-2, and NOX1 with a higher risk of colon cancer.

CONCLUSION

The findings suggest that elevated levels of TNF-α, COX-2, and NOX1 may be associated with the progression of colon cancer, indicating their potential involvement in the disease. Specifically, higher levels of TNF-α and COX-2 could be linked to increased cancer cell proliferation and metastasis, while elevated NOX1 levels might be related to oxidative stress and cellular transformation in colon cancer patients.