【佳學基因檢測】MicroRNA-613 通過 DNA 甲基轉(zhuǎn)移酶 3B/基質(zhì)金屬蛋白酶組織抑制劑 3/信號轉(zhuǎn)導和轉(zhuǎn)錄激活劑 1/叉頭盒 O-1 軸增強鼻咽癌細胞放射敏感性

腫瘤基因檢測公司排名國內(nèi)熱點

與同行交流時知悉《Dis Markers》在.?2022 Aug 26;2022:5699275.發(fā)表了一篇題目為《MicroRNA-613 通過 DNA 甲基轉(zhuǎn)移酶 3B/基質(zhì)金屬蛋白酶組織抑制劑 3/信號轉(zhuǎn)導和轉(zhuǎn)錄激活劑 1/叉頭盒 O-1 軸增強鼻咽癌細胞放射敏感性》腫瘤靶向藥物治療基因檢測臨床研究文章。該研究由Liqiang Deng,?Qing Yin,?Shuyun Liu,?Debao Luo?等完成。促進了腫瘤的正確治療與個性化用藥的發(fā)展，進一步強調(diào)了基因信息檢測與分析的重要性。

腫瘤靶向藥物及正確治療臨床研究內(nèi)容關鍵詞：

腫瘤靶向治療基因檢測臨床應用結果

鼻咽癌（NPC）是鼻咽部常見的惡性腫瘤，抗輻射是鼻咽癌治療的主要障礙。正常細胞的惡性轉(zhuǎn)化是由遺傳和表觀遺傳變化驅(qū)動的，主要表現(xiàn)為 miRNA 水平和 DNA 甲基化狀態(tài)的變化。 microRNA (miR)-613 在多種癌癥中發(fā)揮抑制作用。在此，本研究旨在探索 miR-613 在 NPC 細胞放射敏感性中的作用。檢測鼻咽癌組織中miR-613的表達模式，分析其與臨床指標的相關性。選擇 NP-69 和 C666-1 細胞系進行細胞實驗。通過分級輻射獲得抗輻射細胞系C666-1R。通過CCK-8、集落形成測定和流式細胞術檢測細胞活力、存活分數(shù)和細胞凋亡。 miR-613 和 DNMT3B 之間的結合關系通過雙熒光素酶和 RIP 測定得到驗證。 miR-613在鼻咽癌組織和細胞中低表達，在C666-1R中的表達水平低于C666-1，并進一步與淋巴結轉(zhuǎn)移、腫瘤大小和腫瘤轉(zhuǎn)移相關。 miR-613 過表達降低了 C666-1R 細胞活力和存活率并增加了細胞凋亡，而沉默 miR-613 的 C666-1 細胞呈現(xiàn)相反的趨勢。 miR-613 靶向 DNMT3B。 miR-613 和 DNMT3B 過表達導致 C666-1R 細胞活力和存活率提高，并減少細胞凋亡。 miR-613 通過抑制 DNMT3B 降低 TIMP3 甲基化并提高 TIMP3 蛋白水平。 miR-613 通過抑制 DNMT3B/TIMP3/STAT1/FOXO1 通路增強 NPC 放射敏感性?？傮w而言，miR-613 抑制 DNMT3B，降低 TIMP3 甲基化，增加 TIMP3 蛋白水平，從而抑制 STAT1/FOXO1 通路，增強 NPC 細胞的放射敏感性。

腫瘤發(fā)生與反復轉(zhuǎn)移國際數(shù)據(jù)庫描述：

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.

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