| 王福东,曹 慧,刘 佳.Nemo样激酶促进皮肤鳞状细胞癌增殖和侵袭能力[J].中国肿瘤,2020,29(3):216-222. |
| Nemo样激酶促进皮肤鳞状细胞癌增殖和侵袭能力 |
| Nemo-like Kinase Promotes Proliferation and Invasion of Cutaneous Squamous Cell Carcinoma Cells |
| 中文关键词 修订日期：2019-08-14 |
| DOI：10.11735/j.issn.1004-0242.2020.03.A010 |
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| 中文关键词: 皮肤鳞状细胞癌 Nemo样激酶 增殖 侵袭 JAK1/STAT1信号通路 |
| 英文关键词:cutaneous squamous cell carcinoma nemo-like kinase proliferation invasion JAK1/STAT1 signal pathway |
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| 中文摘要: |
| 摘 要：［目的］ 研究Nemo样激酶(nemo-like kinase，NLK)对皮肤鳞状细胞癌(cutaneous squamous cell carcinoma，CSCC)细胞增殖和侵袭能力的影响，并探讨其作用的可能机制。［方法］ qRT-PCR检测NLK在CSCC细胞系A431、SCL-1、Colo-16和正常永生化的皮肤角质细胞HaCat中的表达，选择表达最高的CSCC细胞系进行NLK干扰慢病毒感染，分为scramble组和sh-NLK组。qRT-PCR检测各组细胞中NLK的表达水平；MTS检测各组细胞增殖活性；平板克隆实验检测各组细胞克隆形成能力；Boyden实验检测各组细胞侵袭能力；皮下移植瘤实验检测各组细胞裸鼠体内成瘤能力；Western blot方法检测NLK对JAK1/STAT1信号通路的影响。采用癌症基因组图谱(The Cancer Genome Atlas，TCGA)数据库分析NLK在皮肤肿瘤组织中的表达情况。［结果］ qRT-PCR检测结果显示NLK mRNA在CSCC细胞系的表达水平均显著高于在正常永生化的皮肤角质细胞HaCat中的表达，选择表达水平最高的A431细胞进行后续实验。qRT-PCR检测发现A431细胞感染NLK干扰慢病毒后，NLK在sh-NLK组中的表达显著降低；sh-NLK组A431细胞增殖活性、平板克隆形成能力、侵袭和裸鼠体内成瘤能力下降，细胞中pJAK1和pSTAT1蛋白的表达降低。TCGA数据库分析结果显示NLK mRNA在皮肤黑色素瘤转移组织中的表达显著高于在原发组织中的表达。［结论］ 干扰NLK的表达可能通过调控JAK1/STAT1信号通路抑制CSCC细胞增殖和侵袭能力。NLK作为CSCC候选癌基因，可能是治疗CSCC的潜在靶点。 |
| 英文摘要: |
| Abstract：［Purpose］ To investigate the effects of nemo-like kinase(NLK) on the proliferation and invasion of cutaneous squamous cell carcinoma(CSCC) cells，and to explore the possible mechanism. ［Methods］ qRT-PCR was used to detect the expression of NLK in CSCC cell lines A431，SCL-1，Colo-16 and normal immortalized skin keratinocyte HaCat cells. The highest expression CSCC cell line was selected for NLK interference lentivirus infection，which was divided into scramble group and sh-NLK group. For each group，qRT-PCR was used to detect the expression level of NLK；MTS was used to detect the proliferation activity；plate clone assay was used to detect the ability to form clones；Boyden test was used to detect the invasive ability；subcutaneous xenografts were used to detect tumor formation ability in mice；Western blot was used to detect the effect of NLK on JAK1/STAT1 signaling pathway. The Cancer Genome Atlas(TCGA) database was used to analyze the expression of NLK in skin tumor tissues. ［Results］The results of qRT-PCR showed that the expression level of NLK mRNA in CSCC cell lines was significantly higher than that in normal immortalized skin keratinocyte HaCat cells. A431 cells with the highest expression level were selected for subsequent experiments. The expression of NLK in sh-NLK group was significantly decreased after A431 cells were infected with NLK interference lentivirus. The proliferation activity，plate cloning ability，invasion and tumorigenic ability and the expression of pJAK1 and pSTAT1 proteins in A431 cells of sh-NLK group were decreased. TCGA database analysis showed that NLK mRNA expression in metastatic skin cutaneous melanoma was significantly higher than that in primary tumors.［Conclusion］ NLK can promote the proliferation and invasion of CSCC cells by regulating JAK1/STAT1 signaling pathway，which indicates that NLK might be used as a potential target for the treatment of CSCC. |
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