| dc.description |
<p>OBJECTIVE: The purpose of our research was to observe the effects of miR-21, miR-221, and miR-222, as well as their target genes on oxidative</p><p>stress, lung cancer formation, and metastasis.</p><p>METHODS: Positron emission tomography/computed tomography, fiberoptic bronchoscopy, and/or endobronchial ultrasonography were performed</p><p>on a total of 69 lung cancer patients to detect the presence or absence of metastasis, and the patients were classified based on the types of cancer.</p><p>Total RNA and miRNA were isolated from the obtained biopsy samples. The quantitative analysis of hsa-miR-21-5p, hsa-miR-222-3p, and hsa-miR-</p><p>221-3p and their target genes was performed by the RT-qPCR method. In determining oxidative stress, total antioxidant status and total oxidant</p><p>status in tissue and total thiol and native thiol in blood were determined spectrophotometrically. OSI and disulfide were calculated.</p><p>RESULTS: We discovered that the metastasis group had higher levels of hsa-miR-21-5p, hsa-miR-221-3p, and hsa-miR-222-3p (p<0.05). While</p><p>TIMP3, PTEN, and apoptotic genes decreased in metastasis, anti-apoptotic genes increased (p<0.05). In addition, while oxidative stress decreased</p><p>in the metastasis group, no change was found in the serum (p>0.05).</p><p>CONCLUSION: Our findings show that upregulation of hsa-miR-21-5p, hsa-miR-221-3p, and hsa-miR-222-3p effectively contributes to both</p><p>proliferation and invasion by influencing oxidative stress and mitochondrial apoptosis.</p> |
|