【佳學(xué)基因檢測(cè)】ATRX 的缺失促進(jìn)骨肉瘤的侵襲性特征，增加 NF-κB 信號(hào)傳導(dǎo)和整合素結(jié)合

夫妻備孕基因檢測(cè)項(xiàng)目要點(diǎn)

體會(huì)記錄《JCI Insight》在.?2022 Sep 8;7(17):e151583.發(fā)表了一篇題目為《ATRX 的缺失促進(jìn)骨肉瘤的侵襲性特征，增加 NF-κB 信號(hào)傳導(dǎo)和整合素結(jié)合》腫瘤靶向藥物治療基因檢測(cè)臨床研究文章。該研究由Suzanne Bartholf DeWitt,?Sarah Hoskinson Plumlee,?Hailey E Brighton,?Dharshan Sivaraj,?E J Martz,?Maryam Zand,?Vardhman Kumar,?Maya U Sheth,?Warren Floyd,?Jacob V Spruance,?Nathan Hawkey,?Shyni Varghese,?Jianhua Ruan,?David G Kirsch,?Jason A Somarelli,?Ben Alman,?William C Eward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：

細(xì)胞遷移/粘附,細(xì)胞外基質(zhì),整合素,腫瘤學(xué)

腫瘤靶向治療基因檢測(cè)臨床應(yīng)用結(jié)果

骨肉瘤 (總生存期) 是一種致命的疾病，很少有已知的靶向療法。在這里，我們表明降低的 ATRX 表達(dá)與更具侵襲性的腫瘤細(xì)胞表型相關(guān)，包括增加的生長(zhǎng)、遷移、侵襲和轉(zhuǎn)移。這些表型變化與 NF-κB 信號(hào)傳導(dǎo)、細(xì)胞外基質(zhì)重塑、整合素 αvβ3 表達(dá)增加和 ETS 家族轉(zhuǎn)錄因子結(jié)合的激活相對(duì)應(yīng)。在這里，我們?cè)隗w外、體內(nèi)和人類 總生存期 患者的數(shù)據(jù)集中描述了這些變化。這種增加的攻擊性實(shí)質(zhì)上使 ATRX 缺陷的 總生存期 細(xì)胞對(duì)整合素信號(hào)傳導(dǎo)抑制敏感。因此，ATRX 在 總生存期 中發(fā)揮重要的腫瘤抑制作用，該基因功能的喪失可能是新的治療漏洞的基礎(chǔ)。 ATRX 表達(dá)與整合素結(jié)合、NF-κB 激活和 ETS 家族轉(zhuǎn)錄因子結(jié)合之間的關(guān)系在先前的研究中沒(méi)有描述，并且可能影響其他 ATRX 缺失疾病的病理生理學(xué)，包括其他癌癥和 ATR-X α 地中海貧血?dú)埣?a href='http://m.vigrxplusreviewsreal.com/about/jishu/33670.html' target='_blank'>綜合征。關(guān)鍵詞：細(xì)胞遷移/粘附；細(xì)胞外基質(zhì)；整合素；腫瘤學(xué)。

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

Osteosarcoma (OS) is a lethal disease with few known targeted therapies. Here, we show that decreased ATRX expression is associated with more aggressive tumor cell phenotypes, including increased growth, migration, invasion, and metastasis. These phenotypic changes correspond with activation of NF-κB signaling, extracellular matrix remodeling, increased integrin αvβ3 expression, and ETS family transcription factor binding. Here, we characterize these changes in vitro, in vivo, and in a data set of human OS patients. This increased aggression substantially sensitizes ATRX-deficient OS cells to integrin signaling inhibition. Thus, ATRX plays an important tumor-suppression role in OS, and loss of function of this gene may underlie new therapeutic vulnerabilities. The relationship between ATRX expression and integrin binding, NF-κB activation, and ETS family transcription factor binding has not been described in previous studies and may impact the pathophysiology of other diseases with ATRX loss, including other cancers and the ATR-X α thalassemia intellectual disability syndrome.Keywords:?Cell migration/adhesion; Extracellular matrix; Integrins; Oncology.