The Effect of MicroRNA-409-3p for Treatment and Response to Tumor Proliferation of Lung Cancer Cell Lines (In Vitro)

Abstract

Objective: Monitoring the result of miR 409 3p and its response to tumor proliferation and its mechanism of action on some types of lung cancer in vitro (A549 cell line). Methods: Two A549 cell line group negative control group with oligonucleotide cultured under conventional conditions and transfected with positive control nucleotides. Experiments Based on the control group, chemically synthesized miR 409 3p mimics were used in the positive group with liposome transfection to construct A549 cells with high miR-409-3p expression. Result: miR4093p expression was estimated using the qPCR method in the two groups after 48 h. Later, the miR-409-3p expression in A549 cells obviously increased significantly with a positive attitude in the positive control group that was transfected by miR-409-3p (mimics) (P<0.20). As a result of this investigation, a significant increase in the percentage of total cell apoptosis was significantly increased in the positive group compared to the control group (22.68% ± 4.62%), (7.79%±1.94%) respectively, (P<0.05). However, in terms of the G1 phase, the rate is obviously low compared to the control group (40.22%±5.36%); (56.08%±5.21%) (P<0.05). endogenous ELF2 was considerably reduced after overexpression of the miR-409-3p mimic (P<0.05). Conclusion: miR-409-3p may prevent non-small cell lung cancer (NSCLC) by affecting ELF2 transcription and other cellular regulators to regulate A549 cell division and induce apoptosis.

Review of multiple sclerosis: Epidemiology, etiology, pathophysiology, and treatment

“…New pathogenic mechanisms, including T-cell entry via the CCR6-CCL20 axis and inhibition of myelination/demyelination via key receptor ligands (e.g., LINGO-1/NOGO66/p75 or TROY complex, Jagged-Notch signaling), have also been identified. [ 13 , 14 ]…”

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“…Previous research indicates that vascular inflammation is significantly influenced by the NF-κB-IL-6 signaling pathway [29]. Furthermore, cisplatin-induced renal injury has been consistently linked with an elevated production of TNF-α in the kidneys [30][31][32][33]. The pro-inflammatory cytokine TNF-α is integral to the inflammation that cisplatin exacerbates.…”

Clinical Pharmacogenetics of Angiotensin II Receptor Blockers in Iraq

“…[ 6 ] Its genetic polymorphism is characterized by variant alleles with reduced activity, CYP2C9 * 2 and CYP2C9 * 3, and the activity of the latter is reduced by almost 90%. [ 20 , 21 ]…”