【佳學(xué)基因檢測】ZEB1：腫瘤轉(zhuǎn)移過程中免疫逃逸的催化劑

基因檢測多少錢解析

閱讀認(rèn)識到《Biomed Pharmacother》在.?2022 Sep;153:113490.發(fā)表了一篇題目為《ZEB1：腫瘤轉(zhuǎn)移過程中免疫逃逸的催化劑》腫瘤靶向藥物治療基因檢測臨床研究文章。該研究由Jiahui Lu,?Fei Fei,?Chenxi Wu,?Jie Mei,?Junying Xu,?Peihua Lu?等完成。促進(jìn)了腫瘤的正確治療與個性化用藥的發(fā)展，進(jìn)一步強(qiáng)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(guān)鍵詞：

急救人員,轉(zhuǎn)移,信號通路,腫瘤免疫,斑馬1

腫瘤靶向治療基因檢測臨床應(yīng)用結(jié)果

轉(zhuǎn)錄因子鋅指 E-box 結(jié)合同源框 1 (ZEB1) 是上皮間充質(zhì)轉(zhuǎn)化 (EMT) 的關(guān)鍵誘導(dǎo)劑，并在腫瘤轉(zhuǎn)移中發(fā)揮重要作用。它不僅可以促進(jìn)腫瘤細(xì)胞的運(yùn)動和擴(kuò)散，還可以促進(jìn)細(xì)胞干性、治療抵抗、腫瘤轉(zhuǎn)移和免疫逃逸。 ZEB1 的表達(dá)受到多種轉(zhuǎn)錄前和轉(zhuǎn)錄后信號通路和分子的嚴(yán)格調(diào)控。越來越多的證據(jù)表明蛋白質(zhì)修飾（例如 ZEB1 的甲基化和乙?；┮部梢杂绊懩[瘤轉(zhuǎn)移。更重要的是，ZEB1誘導(dǎo)免疫抑制細(xì)胞和趨化因子進(jìn)入腫瘤微環(huán)境（TME），導(dǎo)致腫瘤免疫抑制微環(huán)境的形成。本綜述總結(jié)了參與 ZEB1 表達(dá)的調(diào)控因素及其重要作用。本綜述涵蓋的研究領(lǐng)域有助于為惡性腫瘤靶向ZEB1治療提供新思路和新治療見解。轉(zhuǎn)移;信號通路；腫瘤免疫；斑馬1。

腫瘤發(fā)生與反復(fù)轉(zhuǎn)移國際數(shù)據(jù)庫描述：

The transcription factor zinc finger E-box binding homeobox 1 (ZEB1) is a critical inducer of epithelial mesenchymal transformation (EMT) and plays a robust role in tumor metastasis. It can promote not only the movement and diffusion of tumor cells but also cell stemness, treatment resistance, tumor metastasis and immune escape. The expression of ZEB1 is strictly regulated by a variety of pretranscriptional and posttranscriptional signaling pathways and molecules. Increasing evidence indicates that protein modifications such as methylation and acetylation of ZEB1 can also affect tumor metastasis. More importantly, ZEB1 induces immunosuppressive cells and chemokines into the tumor microenvironment (TME), leading to the formation of a tumor immunosuppressive microenvironment. This review summarizes the regulatory factors involved in ZEB1 expression and its important role. The areas of research covered in this review contribute to providing new thoughts and new treatment insights for targeted ZEB1 therapy of malignant tumors.Keywords:?EMT; Metastasis; Signaling pathway; Tumor immunity; ZEB1.