Chen Feng, Jin Yaqiong, Feng Lin, Zhang Jie, Tai Jun, Shi Jin, Yu Yongbo, Lu Jie, Wang Shengcai, Li Xin, Chu Ping, Han Shujing, Cheng Shujun, Guo Yongli, Ni Xin
1Beijing Key Laboratory for Pediatric Diseases of Otolaryngology, Head and Neck Surgery, MOE Key Laboratory of Major Diseases in Children, Beijing Pediatric Research Institute, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing, China.
2Department of Otolaryngology, Head and Neck Surgery, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, No.56 Nanlishi Rd., Beijing, 100045 China.
Cancer Cell Int. 2018 Feb 13;18:20. doi: 10.1186/s12935-018-0519-x. eCollection 2018.
Papillary thyroid carcinoma (PTC) is one of the most frequent malignancies of the endocrine system, whose mechanisms of pathogenesis, progression and prognosis are still far from being clearly elucidated. Despite an increasing body of evidences highlights ribosome biogenesis regulator homolog (RRS1) as a ribosome biogenesis protein in yeast and plants, little is known about human RRS1 function.
Proliferation, cell cycle and apoptosis of PTC cells were assessed following the knockdown of RRS1 expression though MTT, colony formation assay, and flow cytometry. Then, transcriptome profiling was conducted to explore pathway changes after RRS1 silencing in PTC cells. Receiver operating characteristic curve and Youden's index were performed in twenty-four thyroid carcinoma samples to assess their potential clinical diagnostic value.
Firstly, we found that silencing RRS1 significantly reduced cell proliferation, inhibited cell cycle, and promoted apoptosis in PTC cell line. The result also showed that knock-down of RRS1 could up-regulate genes involving apoptosis and metabolism, while, down-regulate genes relative to cell proliferation and blood vessel development. Notably, the present study confirmed the diagnostic value of RRS1 for thyroid carcinoma in both children and adults.
In conclusion, these data afford a comprehensive view of a novel function of human RRS1 by promoting cell proliferation and could be a potential indicator for papillary thyroid carcinoma.
甲状腺乳头状癌（PTC）是内分泌系统最常见的恶性肿瘤之一，其发病机制、进展及预后仍远未明确阐明。尽管越来越多的证据表明核糖体生物合成调节同源物（RRS1）在酵母和植物中是一种核糖体生物合成蛋白，但对人类RRS1的功能知之甚少。
通过MTT法、集落形成试验和流式细胞术，在RRS1表达敲低后评估PTC细胞的增殖、细胞周期和凋亡情况。然后，进行转录组分析以探索PTC细胞中RRS1沉默后的通路变化。在24例甲状腺癌样本中绘制受试者工作特征曲线并计算约登指数，以评估其潜在的临床诊断价值。
首先，我们发现沉默RRS1可显著降低PTC细胞系的细胞增殖，抑制细胞周期，并促进细胞凋亡。结果还表明，敲低RRS1可上调与凋亡和代谢相关的基因，同时下调与细胞增殖和血管发育相关的基因。值得注意的是，本研究证实了RRS1在儿童和成人甲状腺癌中的诊断价值。
总之，这些数据通过促进细胞增殖全面揭示了人类RRS1的新功能，并且可能是甲状腺乳头状癌的一个潜在指标。
