【佳學(xué)基因檢測】生物活性維生素 D 減弱 MED28 介導(dǎo)的人結(jié)直腸癌細胞生長和上皮間質(zhì)轉(zhuǎn)化

基因檢測的費用是多少詳解

討化《腫瘤靶向藥物選擇的基因突變標準》《Biomed Res Int》在.?2022 Aug 29;2022:2268818.發(fā)表了一篇題目為《生物活性維生素 D 減弱 MED28 介導(dǎo)的人結(jié)直腸癌細胞生長和上皮間質(zhì)轉(zhuǎn)化》腫瘤靶向藥物治療基因檢測臨床研究文章。該研究由Chun-Yin Huang,?Yu-Ting Weng,?Nien-Tsu Hsieh,?Po-Chen Li,?Tzu-Yi Lee,?Chun-I Li,?Hsiao-Sheng Liu,?Ming-Fen Lee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(guān)鍵詞：

腫瘤靶向治療基因檢測臨床應(yīng)用結(jié)果

維生素 D 狀態(tài)不足可能會增加患多種癌癥的風(fēng)險。流行病學(xué)研究表明 25-羥基維生素 D3 (25(OH)D3) 與包括結(jié)直腸癌在內(nèi)的惡性腫瘤之間存在負相關(guān)。以前的研究表明，MED28 是一種參與轉(zhuǎn)錄調(diào)控的介質(zhì)亞基，與結(jié)直腸癌細胞的生長有關(guān)。然而，目前尚不清楚其在結(jié)直腸癌上皮間質(zhì)轉(zhuǎn)化（EMT）和細胞遷移等轉(zhuǎn)移進展中的作用。本研究的目的是研究骨化三醇、1,25-二羥基維生素 D3 (1,25(OH)2D3)（一種維生素 D 的生物活性形式）的潛在抑制作用，以及 MED28 在人類 EMT 進展中的作用大腸癌細胞。 MED28 的抑制增加了 E-cadherin 的表達并降低了幾種間充質(zhì)和遷移生物標志物以及 Wnt/β-catenin 信號分子的表達，而 MED28 的過表達增強了 EMT 特征。骨化三醇抑制 MED28 的表達，骨化三醇的作用反映了 MED28 沉默的作用。我們的數(shù)據(jù)表明，骨化三醇減弱了人類結(jié)直腸癌細胞中 MED28 介導(dǎo)的細胞生長和 EMT，強調(diào)了 MED28 在結(jié)直腸癌進展中的重要性并支持骨化三醇的潛在轉(zhuǎn)化應(yīng)用。

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

Inadequate vitamin D status may increase the risk of developing multiple types of cancer. Epidemiological studies suggest an inverse association between 25-hydroxyvitamin D3?(25(OH)D3) and malignancy, including colorectal cancer. Previous studies have suggested that MED28, a Mediator subunit involved in transcriptional regulation, is associated with the growth of colorectal cancer cells; however, its role in the progression of metastasis such as epithelial-mesenchymal transition (EMT) and cell migration of colorectal cancer is unclear at present. The aim of this study was to investigate a potentially suppressive effect of calcitriol, 1,25-dihydroxyvitamin D3?(1,25(OH)2D3), a bioactive form of vitamin D, and the role of MED28 in the progression of EMT in human colorectal cancer cells. Suppression of MED28 increased the expression of E-cadherin and reduced the expression of several mesenchymal and migration biomarkers and Wnt/β-catenin signaling molecules, whereas overexpression of MED28 enhanced the EMT features. Calcitriol suppressed the expression of MED28, and the effect of calcitriol mirrored that of MED28 silencing. Our data indicate that calcitriol attenuated MED28-mediated cell growth and EMT in human colorectal cancer cells, underlining the significance of MED28 in the progression of colorectal cancer and supporting the potential translational application of calcitriol.

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