Curcumin Increases Radiosensitivity of Radioresistant Nasopharyngeal Cancer.

IF 2 4区 医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
Guoyu Wang, Jie Zhu, Zengxian Wang, Zuliang Xu, Yiming Shi, Lingjie Luo
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引用次数: 1

Abstract

Objectives: To study the effects of curcumin on the proliferation, invasion, apoptosis, and radiosensitivity of the radioresistant nasopharyngeal carcinoma (NPC) C6661-IR strain as well as the potential radiosensitization mechanism.

Methods: NPC cells were continuously irradiated with different intensities of radiation to induce radiation-resistant cell lines. A plate clone formation assay was used to evaluate the effect of curcumin on the radiosensitivity of NPC cells. 3-(4,5-Dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide thiazolyl blue (MTT) assay was conducted to detect changes in cell viability. Flow cytometry was employed to analyze apoptosis percentage as well as Transwell® assay and immunofluorescence assay to observe cell invasion. Western blotting was applied to detect the expression levels of Bax, Bcl-2, and pro/cleaved-caspase 3. MiR-205-5p mimics and si-TP53INP1 were synthesized and transfected into C6661-IR cells, and the cells were then incubated with 10 μm/L curcumin. Real-time quantitative reverse transcription PCR (RT-qPCR) was used to measure miR-205-5p levels and western blotting was conducted to detect the expression of TP53INP1.

Results: The optimal radiation dose of X-ray was 6 Gy, and this dose was used in all subsequent experiments. Curcumin treatment significantly inhibited the proliferation and invasion of C6661-IR cells, promoted apoptosis and enhanced radiosensitivity. Compared to the 0 Gy+Cur group and the 6 Gy+Cur group, the miR-205-5p levels were higher in the C6661-IR cells of the 0 Gy and 6 Gy groups. Moreover, miR-204-5p was found to directly target TP53INP1. Curcumin downregulated miR-205-5p levels and upregulated TP53INP1 expression (p < 0.05). Thus, modulation of miR-205-5p or TP53INP1 expression attenuates the biological effects of curcumin on C6661-IR cells.

Conclusions: Curcumin inhibited the proliferation and invasion of C6661-IR, promoted apoptosis, and enhanced its radiosensitivity to X-rays by mediating miR-205-5p/TP53INP1 expression.

姜黄素增加放射耐药鼻咽癌的放射敏感性。
目的:研究姜黄素对鼻咽癌(NPC) C6661-IR耐药菌株增殖、侵袭、凋亡及放射敏感性的影响及其可能的致敏机制。方法:用不同强度的辐射连续照射鼻咽癌细胞,诱导抗辐射细胞系。采用平板克隆形成法观察姜黄素对鼻咽癌细胞放射敏感性的影响。采用3-(4,5-二甲基噻唑-2基)-2,5-二苯基溴化四唑噻唑蓝(MTT)法检测细胞活力的变化。流式细胞术检测细胞凋亡率,Transwell®法和免疫荧光法观察细胞侵袭情况。Western blotting检测Bax、Bcl-2、pro/cleaved-caspase 3的表达水平。合成MiR-205-5p模拟物和si-TP53INP1转染到C6661-IR细胞中,用10 μm/L姜黄素孵育细胞。采用实时定量反转录PCR (RT-qPCR)检测miR-205-5p水平,western blotting检测TP53INP1的表达。结果:x射线的最佳照射剂量为6 Gy,后续实验均采用该剂量。姜黄素处理显著抑制C6661-IR细胞的增殖和侵袭,促进细胞凋亡,增强放射敏感性。与0 Gy+Cur组和6 Gy+Cur组相比,0 Gy和6 Gy组C6661-IR细胞中miR-205-5p水平更高。此外,miR-204-5p被发现直接靶向TP53INP1。姜黄素下调miR-205-5p水平,上调TP53INP1表达(p < 0.05)。因此,调节miR-205-5p或TP53INP1表达可减弱姜黄素对C6661-IR细胞的生物学效应。结论:姜黄素通过介导miR-205-5p/TP53INP1的表达,抑制C6661-IR的增殖和侵袭,促进细胞凋亡,增强其对x射线的放射敏感性。
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来源期刊
Discovery medicine
Discovery medicine MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
5.40
自引率
0.00%
发文量
80
审稿时长
6-12 weeks
期刊介绍: Discovery Medicine publishes novel, provocative ideas and research findings that challenge conventional notions about disease mechanisms, diagnosis, treatment, or any of the life sciences subjects. It publishes cutting-edge, reliable, and authoritative information in all branches of life sciences but primarily in the following areas: Novel therapies and diagnostics (approved or experimental); innovative ideas, research technologies, and translational research that will give rise to the next generation of new drugs and therapies; breakthrough understanding of mechanism of disease, biology, and physiology; and commercialization of biomedical discoveries pertaining to the development of new drugs, therapies, medical devices, and research technology.
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