【佳学基因检测】MicroRNA-613 通过 DNA 甲基转移酶 3B/基质金属蛋白酶组织抑制剂 3/信号转导和转录激活剂 1/叉头盒 O-1 轴增强鼻咽癌细胞放射敏感性

肿瘤基因检测公司排名国内热点

与同行交流时知悉《Dis Markers》在. 2022 Aug 26;2022:5699275.发表了一篇题目为《MicroRNA-613 通过 DNA 甲基转移酶 3B/基质金属蛋白酶组织抑制剂 3/信号转导和转录激活剂 1/叉头盒 O-1 轴增强鼻咽癌细胞放射敏感性》肿瘤靶向药物治疗基因检测临床研究文章。该研究由Liqiang Deng, Qing Yin, Shuyun Liu, Debao Luo 等完成。促进了肿瘤的正确治疗与个性化用药的发展，进一步强调了基因信息检测与分析的重要性。

肿瘤靶向药物及正确治疗临床研究内容关键词：

肿瘤靶向治疗基因检测临床应用结果

鼻咽癌（NPC）是鼻咽部常见的恶性肿瘤，抗辐射是鼻咽癌治疗的主要障碍。正常细胞的恶性转化是由遗传和表观遗传变化驱动的，主要表现为 miRNA 水平和 DNA 甲基化状态的变化。 microRNA (miR)-613 在多种癌症中发挥抑制作用。在此，本研究旨在探索 miR-613 在 NPC 细胞放射敏感性中的作用。检测鼻咽癌组织中miR-613的表达模式，分析其与临床指标的相关性。选择 NP-69 和 C666-1 细胞系进行细胞实验。通过分级辐射获得抗辐射细胞系C666-1R。通过CCK-8、集落形成测定和流式细胞术检测细胞活力、存活分数和细胞凋亡。 miR-613 和 DNMT3B 之间的结合关系通过双荧光素酶和 RIP 测定得到验证。 miR-613在鼻咽癌组织和细胞中低表达，在C666-1R中的表达水平低于C666-1，并进一步与淋巴结转移、肿瘤大小和肿瘤转移相关。 miR-613 过表达降低了 C666-1R 细胞活力和存活率并增加了细胞凋亡，而沉默 miR-613 的 C666-1 细胞呈现相反的趋势。 miR-613 靶向 DNMT3B。 miR-613 和 DNMT3B 过表达导致 C666-1R 细胞活力和存活率提高，并减少细胞凋亡。 miR-613 通过抑制 DNMT3B 降低 TIMP3 甲基化并提高 TIMP3 蛋白水平。 miR-613 通过抑制 DNMT3B/TIMP3/STAT1/FOXO1 通路增强 NPC 放射敏感性。总体而言，miR-613 抑制 DNMT3B，降低 TIMP3 甲基化，增加 TIMP3 蛋白水平，从而抑制 STAT1/FOXO1 通路，增强 NPC 细胞的放射敏感性。

肿瘤发生与反复转移国际数据库描述：

Nasopharyngeal carcinoma (NPC) is a common malignancy of the nasopharynx, and radioresistant represents the main obstacle in NPC treatment. Malignant transformation of normal cells is driven by genetic and epigenetic changes, which are primarily manifested as changes in miRNA levels and DNA methylation status. microRNA (miR)-613 plays an inhibitory role in several types of cancer. Herein, the current study sought to explore the roles of miR-613 in NPC cell radiosensitivity. miR-613 expression patterns in NPC tissues were detected, and its correlation with clinical indexes was analyzed. NP-69 and C666-1 cell lines were selected for cellular experimentation. Radioresistant cell line C666-1R was obtained by fractionated radiation. Cell viability, survival fraction, and apoptosis were detected by CCK-8, colony formation assay, and flow cytometry. The binding relation between miR-613 and DNMT3B was verified by dual-luciferase and RIP assays. miR-613 was lowly expressed in NPC tissues and cells, with lower expression levels in C666-1R than C666-1, and further correlated with lymph node metastasis, tumor size, and tumor metastasis. miR-613 overexpression reduced C666-1R cell viability and survival fraction and increased apoptosis, while C666-1 cells with silencing miR-613 presented the opposite trends. miR-613 targeted DNMT3B. miR-613 and DNMT3B overexpression led to enhanced C666-1R cell viability and survival fraction and decreased apoptosis. miR-613 reduced TIMP3 methylation and elevated TIMP3 protein level by inhibiting DNMT3B. miR-613 enhanced NPC radiosensitivity by inhibiting the DNMT3B/TIMP3/STAT1/FOXO1 pathway. Collectively, miR-613 inhibited DNMT3B, reduced TIMP3 methylation, and increased TIMP3 protein level, thus inhibiting the STAT1/FOXO1 pathway and enhancing the radiosensitivity of NPC cells.