miR-21, miR-221, and miR-222 upregulation in lung cancer promotes metastasis by reducing oxidative stress and apoptosis
REVISTA DA ASSOCIACAO MEDICA BRASILEIRA, cilt.69, sa.6, ss.1-5, 2023 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 69 Sayı: 6
- Basım Tarihi: 2023
- Doi Numarası: 10.1590/1806-9282.20221688
- Dergi Adı: REVISTA DA ASSOCIACAO MEDICA BRASILEIRA
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, CAB Abstracts, EMBASE, MEDLINE, Veterinary Science Database, Directory of Open Access Journals
- Sayfa Sayıları: ss.1-5
- Süleyman Demirel Üniversitesi Adresli: Evet
Özet
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
stress, lung cancer formation, and metastasis.
METHODS: Positron emission tomography/computed tomography, fiberoptic bronchoscopy, and/or endobronchial ultrasonography were performed
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.
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-
221-3p and their target genes was performed by the RT-qPCR method. In determining oxidative stress, total antioxidant status and total oxidant
status in tissue and total thiol and native thiol in blood were determined spectrophotometrically. OSI and disulfide were calculated.
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
TIMP3, PTEN, and apoptotic genes decreased in metastasis, anti-apoptotic genes increased (p<0.05). In addition, while oxidative stress decreased
in the metastasis group, no change was found in the serum (p>0.05).
CONCLUSION: Our findings show that upregulation of hsa-miR-21-5p, hsa-miR-221-3p, and hsa-miR-222-3p effectively contributes to both
proliferation and invasion by influencing oxidative stress and mitochondrial apoptosis.