【佳學(xué)基因檢測(cè)】FOXD1 通過(guò)調(diào)節(jié) GLUT1 介導(dǎo)的有氧糖酵解促進(jìn)胰腺癌細(xì)胞增殖、侵襲和轉(zhuǎn)移

靶向藥一般多少錢排名

研究看到《Cell Death Dis》在.?2022 Sep 3;13(9):765.發(fā)表了一篇題目為《FOXD1 通過(guò)調(diào)節(jié) GLUT1 介導(dǎo)的有氧糖酵解促進(jìn)胰腺癌細(xì)胞增殖、侵襲和轉(zhuǎn)移》腫瘤靶向藥物治療基因檢測(cè)臨床研究文章。該研究由Kun Cai?#,?Shiyu Chen?#,?Changhao Zhu?#,?Lin Li,?Chao Yu,?Zhiwei He,?Chengyi Sun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

盡管已發(fā)現(xiàn) FOXD1 參與多種癌癥的惡性過(guò)程，但其在胰腺癌 (PC) 中的作用尚不清楚。本研究旨在探討FOXD1在PC中的表達(dá)和功能。我們發(fā)現(xiàn)與非腫瘤組織相比，PC 組織中 FOXD1 的 mRNA 和蛋白表達(dá)上調(diào)，并且 FOXD1 的高表達(dá)水平與 PC 的不良預(yù)后指數(shù)相關(guān)。體外和體內(nèi)測(cè)定結(jié)果表明，F(xiàn)OXD1 的過(guò)表達(dá)促進(jìn)有氧糖酵解和 PC 細(xì)胞增殖、侵襲和轉(zhuǎn)移的能力，而 FOXD1 敲低抑制這些功能。機(jī)理實(shí)驗(yàn)結(jié)果表明，F(xiàn)OXD1不僅可以直接促進(jìn)SLC2A1的轉(zhuǎn)錄，還可以通過(guò)RNA誘導(dǎo)的沉默復(fù)合物抑制SLC2A1的降解。因此，F(xiàn)OXD1 增強(qiáng) GLUT1 表達(dá)，并賊終通過(guò)調(diào)節(jié)有氧糖酵解促進(jìn) PC 細(xì)胞增殖、侵襲和轉(zhuǎn)移?？傊現(xiàn)OXD1 被認(rèn)為是 PC 的潛在治療靶點(diǎn)。

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

Although FOXD1 has been found to be involved in the malignant processes of several types of cancers, its role in pancreatic cancer (PC) is not well understood. This study aimed to investigate the expression and function of FOXD1 in PC. We found that FOXD1 mRNA and protein expression were upregulated in PC tissues compared with non-tumor tissues, and high expression level of FOXD1 was associated with an adverse prognostic index of PC. The results of in vitro and in vivo assays indicate that overexpression of FOXD1 promotes aerobic glycolysis and the capacity of PC cells to proliferate, invade, and metastasize, whereas FOXD1 knockdown inhibits these functions. The results of mechanistic experiments suggest that FOXD1 can not only directly promote SLC2A1 transcription but also inhibit the degradation of SLC2A1 through the RNA-induced silencing complex. As a result, FOXD1 enhances GLUT1 expression and ultimately facilitates PC cell proliferation, invasion, and metastasis by regulating aerobic glycolysis. Taken together, FOXD1 is suggested to be a potential therapeutic target for PC.