沉默长链非编码RNA MCM3AP-AS1可保护A549肺癌细胞免受顺铂诱导的细胞死亡。
Silencing lncRNA MCM3AP-AS1 protects against cisplatin-induced cell death in A549 lung cancer cells.
作者信息
Bozgeyik Ibrahim, Tasdemir Demet, Bozgeyik Esra, Bagis Haydar, Oztuzcu Serdar, Isik Ahmet Ferudun
机构信息
Department of Medical Biology, Faculty of Medicine, Adiyaman University, 02040, Adiyaman, Turkey.
Respiratory Diseases and Respiratory Surgery Research and Practice Center, Gaziantep University, Gaziantep, Turkey.
出版信息
Mol Biol Rep. 2025 Jul 14;52(1):708. doi: 10.1007/s11033-025-10822-7.
BACKGROUND
Lung cancer remains the leading cause of cancer-related mortality worldwide, largely due to the development of resistance to standard chemotherapeutic agents such as cisplatin. Recent evidence has highlighted the regulatory role of long non-coding RNAs (lncRNAs) in mediating drug resistance mechanisms. In this study, we aimed to reveal the role of MCM3AP-AS1 in cisplatin-induced cell death in lung cancer cells.
METHODS AND RESULTS
As a result, we found that MCM3AP-AS1, a lncRNA previously associated with poor prognosis in various cancers, was significantly upregulated in A549 lung cancer cells following cisplatin treatment. Using RNA interference-mediated silencing of MCM3AP-AS1, we observed a marked increase in cell viability and a decrease in apoptosis, as determined by MTT assay, annexin V/PI flow cytometry, and acridine orange/ethidium bromide staining.
CONCLUSIONS
These findings suggest that MCM3AP-AS1 may be a crucial modulator of cisplatin-induced apoptosis in lung cancer cells.
背景
肺癌仍是全球癌症相关死亡的主要原因，这主要归因于对顺铂等标准化疗药物产生耐药性。最近的证据凸显了长链非编码RNA（lncRNA）在介导耐药机制中的调节作用。在本研究中，我们旨在揭示MCM3AP-AS1在顺铂诱导肺癌细胞死亡中的作用。
方法与结果
结果发现，MCM3AP-AS1是一种先前与多种癌症预后不良相关的lncRNA，在顺铂处理后的A549肺癌细胞中显著上调。通过RNA干扰介导沉默MCM3AP-AS1，我们观察到细胞活力显著增加，凋亡减少，这通过MTT法、膜联蛋白V/碘化丙啶流式细胞术和吖啶橙/溴化乙锭染色得以确定。
结论
这些发现表明，MCM3AP-AS1可能是顺铂诱导肺癌细胞凋亡的关键调节因子。
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