| 郑泽轩,沈嘉浩,裴海龙,等.PLIN5通过介导脂滴累积增加非小细胞肺癌细胞辐射抗性[J].中华放射医学与防护杂志,2026,46(5):483-489.Zheng Zexuan,Shen Jiahao,Pei Hailong,et al.PLIN5 enhances radioresistance in non-small cell lung cancer cells by mediating the accumulation of lipid droplets[J].Chin J Radiol Med Prot,2026,46(5):483-489 |
| PLIN5通过介导脂滴累积增加非小细胞肺癌细胞辐射抗性 |
| PLIN5 enhances radioresistance in non-small cell lung cancer cells by mediating the accumulation of lipid droplets |
| 投稿时间：2025-09-18 |
| DOI：10.3760/cma.j.cn112271-20250918-00336 |
| 中文关键词: 脂滴包被蛋白5 中性脂质 非小细胞肺癌 辐射敏感性 |
| 英文关键词:Perilipin 5 Neutral lipids Non-small cell lung cancer Radiosensitivity |
| 基金项目:国家自然科学基金(82273578) |
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| 中文摘要: |
| 目的 探究脂滴包被蛋白5(PLIN5)对于非小细胞肺癌细胞中性脂质含量及其辐射敏感性的影响及机制。方法 对非小细胞肺癌细胞系A549和Calu-1进行0和2 Gy X射线照射,通过基因表达差异分析和荧光定量PCR检测两组细胞的PLIN5基因表达水平。构建PLIN5全长和成脂结构域截断体过表达细胞系以及PLIN5基因敲减细胞系,以野生型细胞系和空载质粒转染的细胞系为对照组,分别进行0和8 Gy X射线照射,采用CCK-8方法检验各组细胞的活力,绘制细胞相对增殖速率曲线;通过流式细胞术检测细胞凋亡;照后24 h,分别用BODIPY594和HOCHEST染色,在共聚焦显微镜下拍摄观察脂质表达水平。结果 2 Gy X射线照射后A549细胞产生差异表达基因487个,qPCR验证显示PLIN5基因表达水平较对照组升高2.5倍(t=3.06,P<0.05)。8 Gy X射线照射后,PLIN5全长转染组的细胞脂质表达水平较野生型细胞高,PLIN5干扰组的细胞脂质表达水平较野生型细胞低,删除PLIN5成脂结构域的截断体脂质含量无显著变化。与空载体照射组细胞活力(1.69±0.49)%相比,PLIN5全长过表达组的细胞活力提高至(2.49±0.92)%(t=2.64,P<0.05);与阴性对照照射组细胞活力(2.54±0.80)%相比,PLIN5干扰组的细胞活力降至(1.89±0.45)%(t=3.76,P<0.05),而删除PLIN5成脂结构域的截断体转染组、野生型、空载质粒转染组比较差异无统计学意义。结论 在辐射条件下PLIN5的表达增加提高了A549细胞的脂质水平,从而提高细胞的辐射抗性,为脂质代谢重编程在肿瘤细胞辐射抗性中的关键作用提供了依据。 |
| 英文摘要: |
| Objective To investigate the effect of perilipin 5 (PLIN5) on neutral lipid content and radiosensitivity in non-small cell lung cancer (NSCLC) cells and its underlying mechanism. Methods The NSCLC cell line A549 was irradiated with 0 or 2 Gy of X-rays. PLIN5 gene expression levels in the two groups were detected via differential gene expression analysis and quantitative real-time PCR (qPCR). Cell lines stably overexpressing full-length PLIN5 or a truncated mutant lacking the lipid-binding domain, as well as PLIN5 knockdown cell lines, were constructed. Wild-type cells and empty vector-transfected cells served as controls. These cell groups were irradiated with 0 Gy or 8 Gy of X-rays. Relative cell proliferation rate curve and cell apoptosis was assessed. At 24 h post-irradiation, cells were stained with BODIPY 594 and Hoechst, and observed under a confocal microscope to evaluate lipid expression levels. Results After 2 Gy X-ray irradiation, 487 differentially expressed genes were identified in A549 cells. qPCR validation showed that PLIN5 expression increased by 2.5-fold compared to the control group (t=3.06, P<0.05). Following 8 Gy irradiation, lipid expression levels were higher in the full-length PLIN5 overexpression group and lower in the PLIN5 knockdown group compared to wild-type cells. The truncated mutant lacking the lipid-binding domain showed no significant change in lipid content. Compared with the cell viability of (1.69±0.49)% in the empty vector irradiation group, the cell viability of the PLIN5 full-length overexpression group increased to (2.49±0.92)% (t=2.64, P<0.05). Compared with the cell viability of (2.54±0.80)% in the negative control exposure group, the cell viability of the PLIN5 interference group decreased to (1.89±0.45)% (t=3.76, P<0.05). No statistically significant difference was observed among the truncated mutant transfection group, wild-type cells, and the empty vector transfection group. Conclusions Under irradiation, up-regulated PLIN5 elevates lipid content in A549 cells, thereby enhancing their radioresistance and providing evidence that lipid-metabolic reprogramming is a critical determinant of tumor cell radioresistance. |
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