Investigation of the effects of rps26p25 pseudogene on cell viability, apoptosis and cell cycle in lung cancer

Objective: This study aimed to investigate the potential role of the pseudogene RPS26P25 in lung cancer cells and to evaluate its applicability as a therapeutic target. Materials and Methods: Human lung adenocarcinoma cell line (A549) and healthy Type II alveolar epithelial cells were used. Cells were cultured in MEM medium, and viability was monitored by trypan blue exclusion. RPS26P25 expression was determined by qPCR, and gene silencing was performed using siRNA. Following transfection, RNA isolation and qPCR were used to verify silencing efficiency. Apoptosis and cell cycle analyses were conducted via flow cytometry. Combination treatments with cisplatin were also performed. Data were analyzed using GraphPad Prism software. Results: The silencing of the RPS26P25 pseudogene resulted in a significant increase of 16.07% in the total apoptotic cell rate in A549 cells (p < 0.0001); its combination with cisplatin provided an additional 4.65% increase, but this difference was not found to be statistically significant (p = 0.1016). In T2A cells, apoptosis increased by 6.69% (p = 0.0101), while the combination led to a 5.32% decrease (p = 0.052). In cell cycle analysis, an increase in the G0/G1 phase was observed in A549 cells (p = 0.0137), accompanied by a decrease in the S phase. Cisplatin caused accumulation in the S phase (p < 0.0001), and this effect was not altered by gene silencing. In T2A cells, none of the treatments induced significant changes in the G1, S, or G2 phases (p > 0.05). Conclusion: RPS26P25 was shown to influence apoptosis and chemosensitivity in lung cancer cells. These findings suggest that this pseudogene may serve as a therapeutic target and a potential biomarker in lung cancer. Further in vivo and clinical studies are needed to elucidate its role in cellular signaling pathways and confirm its translational relevance. Keywords:Apoptosis, Cell Viability, Cisplatin, Lung Cancer, Pseudogene, RNA Interference