【佳學(xué)基因檢測(cè)】缺氧誘導(dǎo)的巢蛋白通過(guò)靶向轉(zhuǎn)錄因子 Nrf2、STAT3 和 SOX2 調(diào)節(jié)肺癌的活力和代謝

腫瘤基因檢測(cè)多少錢原理

學(xué)習(xí)認(rèn)識(shí)到《Comput Intell Neurosci》在.?2022 Aug 30;2022:9811905.發(fā)表了一篇題目為《缺氧誘導(dǎo)的巢蛋白通過(guò)靶向轉(zhuǎn)錄因子 Nrf2、STAT3 和 SOX2 調(diào)節(jié)肺癌的活力和代謝》腫瘤靶向藥物治療基因檢測(cè)臨床研究文章。該研究由Yongshi Liu,?Xinglin Zhang,?Tao Jiang,?Ning Du?等完成。促進(jìn)了腫瘤的正確治療與個(gè)性化用藥的發(fā)展，進(jìn)一步強(qiáng)調(diào)了基因信息檢測(cè)與分析的重要性。

腫瘤靶向藥物及正確治療臨床研究?jī)?nèi)容關(guān)鍵詞：

腫瘤靶向治療基因檢測(cè)臨床應(yīng)用結(jié)果

目的：探討低氧誘導(dǎo)的Nestin通過(guò)靶向轉(zhuǎn)錄因子Nrf2、STAT3和SOX2調(diào)控肺癌細(xì)胞活力和代謝。方法：84例非小細(xì)胞肺癌（nonsmall cell lung cancer, NSCLC）治療2020 年 6 月至 2021 年 2 月，從我們的臨床病理學(xué)數(shù)據(jù)庫(kù)中隨機(jī)選擇。對(duì)收集的組織細(xì)胞進(jìn)行免疫組織化學(xué)染色，以評(píng)估巢蛋白、STAT3、Nrf2 和 SOX2 的表達(dá)模式。使用單因素和雙因素方差分析對(duì)數(shù)據(jù)進(jìn)行量化和統(tǒng)計(jì)分析，P < 0.05。 Nestin表達(dá)與STAT3、Nrf2、SOX2表達(dá)相關(guān)。Nestin/STAT3/SOX2/Nrf2參與血管生成和肺癌發(fā)生發(fā)展。結(jié)論：缺氧誘導(dǎo)的Nestin通過(guò)靶向下游轉(zhuǎn)錄因子STAT3促進(jìn)非小肺癌細(xì)胞的進(jìn)展， Nrf2 和 SOX2。

腫瘤發(fā)生與反復(fù)轉(zhuǎn)移國(guó)際數(shù)據(jù)庫(kù)描述：

Objective:?To investigate hypoxia-induced Nestin regulates lung cancer viability and metabolism by targeting transcription factors Nrf2, STAT3, and SOX2.Methods:?Eighty-four cases of nonsmall cell lung cancer (nonsmall cell lung cancer, NSCLC), which had been treated from June 2020 to February 2021, were randomly selected from our clinicopathology database. Immunohistochemical staining of collected tissue cells was performed to assess the expression patterns of Nestin, STAT3, Nrf2, and SOX2. Data were quantified and statistically analyzed using one-way and two-way ANOVA tests with?P?< 0.05.Results:?Clinicopathological findings showed significant differences in lymph node metastasis, tissue differentiation, and histology on induction of Nestin expression; Nestin expression correlated with STAT3, Nrf2, and SOX2 expression.Nestin/STAT3/SOX2/Nrf2 are involved in angiogenesis and lung cancer development.Conclusion:?Hypoxia-induced Nestin promotes the progression of nonsmall lung cancer cells by targeting the downstream transcription factors STAT3, Nrf2, and SOX2.