氨酸通过 lncRNA CBR3-AS1 影响骨髓瘤细胞的免疫活性
Wenpeng Xie1, Fengjun Ma2, Luming Dou3
1Department of Orthopedics, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, 250014, China.
Heliyon
|July 1, 2024
概括
氨酸通过向CBR3-AS1/miR-145-5p/GRP78通路来增强骨髓瘤 (OS) 免疫活性和亡. 这项研究提供了对艾利辛的证据.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- 骨髓瘤 (OS) 是一种具有复杂免疫活性的原发性骨恶性瘤.
- 了解OS进展和免疫逃避背后的分子机制对于开发有效疗法至关重要.
研究的目的:
- 为了研究素对骨髓瘤细胞免疫活性的影响.
- 阐明长非编码RNA (lncRNA) CBR3-AS1/miR-145-5p/GRP78轴在素作用机制中的作用.
- 为艾利作为OS中的免疫调节剂提供潜在的临床证据.
主要方法:
- 在体外研究中,使用 Saos-2 人类 OS 细胞系治疗了不同度的素.
- 感染CBR3-AS1异常表达载体以评估其对OS细胞的影响.
- 救援实验以验证CBR3-AS1/miR-145-5p/GRP78轴内的监管关系.
- 在裸体小鼠的体内瘤生成实验中,评估艾利对瘤生长和T淋巴细胞子集的影响.
主要成果:
- 阿利治疗降低了Saos-2细胞活性,并以剂量依赖的方式增加了亡.
- 氨酸调节了关键分子的表达:降低CBR3-AS1和GRP78,同时增加miR-145-5p.
- 沉默CBR3-AS1模仿了阿利的作用,减少了细胞活性,增强了细胞亡,线粒和内细胞网膜压力.
- 救援实验证实了调节轴:CBR3-AS1通过miR-145-5p影响OS细胞,miR-145-5p的影响由GRP78.8介导.
- 在体内研究表明,氨酸和确定的分子轴调节瘤生长,氨酸激活CD4+CD8+T细胞,表明增强的免疫活性.
结论:
- 阿利有效地激活骨髓瘤免疫活性,并诱导亡.
- 该机制涉及对lncRNA CBR3-AS1/miR-145-5p/GRP78分子轴的调制.
- 这些发现支持阿利因作为治疗骨髓瘤的治疗剂的潜力,通过增强抗瘤免疫力.
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