【佳學(xué)基因檢測】Sam68的高表達(dá)通過調(diào)節(jié)波形蛋白表達(dá)和口腔鱗狀細(xì)胞癌的運(yùn)動表型促進(jìn)轉(zhuǎn)移

基因突變癲瘋病會好嗎排隊

分析基因檢測與基因解碼的區(qū)別與選擇體會到《Oncol Rep》在.?2022 Oct;48(4):183.發(fā)表了一篇題目為《Sam68的高表達(dá)通過調(diào)節(jié)波形蛋白表達(dá)和口腔鱗狀細(xì)胞癌的運(yùn)動表型促進(jìn)轉(zhuǎn)移》腫瘤靶向藥物治療基因檢測臨床研究文章。該研究由Takuya Komiyama,?Takeshi Kuroshima,?Takehito Sugasawa,?Shin-Ichiro Fujita,?Yuta Ikami,?Hideaki Hirai,?Fumihiko Tsushima,?Yasuyuki Michi,?Kou Kayamori,?Fumihiro Higashino,?Hiroyuki Harada?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：

Src 相關(guān)的有絲分裂 68 kDa,上皮間質(zhì)轉(zhuǎn)化,轉(zhuǎn)移,動力,口腔癌,波形蛋白

腫瘤靶向治療基因檢測臨床應(yīng)用結(jié)果

本研究旨在探討 Src 相關(guān)的有絲分裂 68 kDa (Sam68) 在口腔鱗狀細(xì)胞癌 (總生存期CC) 中的臨床和生物學(xué)意義。對從 77 名 總生存期CC 患者獲得的組織樣本進(jìn)行免疫組織化學(xué)分析。單因素分析顯示，Sam68的高表達(dá)與晚期病理T分期（P=0.01）、陽性淋巴血管浸潤（P=0.01）、病理性頸淋巴結(jié)轉(zhuǎn)移（P<0.01）顯著相關(guān)。此外，多因素分析表明，Sam68 的高表達(dá)是頸部淋巴結(jié)轉(zhuǎn)移的獨(dú)立預(yù)測因素（優(yōu)勢比，4.39；95% 置信區(qū)間，1.49-14.23；P<0.01）。這些結(jié)果表明，Sam68 的高表達(dá)有助于 總生存期CC 中的腫瘤進(jìn)展，尤其是頸部淋巴結(jié)轉(zhuǎn)移。還進(jìn)行了 mRNA 測序以評估具有 Sam68 敲低的 總生存期CC 細(xì)胞和對照細(xì)胞之間轉(zhuǎn)錄組的變化，目的是闡明 Sam68 的生物學(xué)作用?；虮倔w富集分析表明，下調(diào)的差異表達(dá)基因（DEGs）集中在一些與上皮-間質(zhì)轉(zhuǎn)化相關(guān)的生物學(xué)過程中。在這些 DEG 中，確定波形蛋白在這些細(xì)胞中特別下調(diào)。還證實 Sam68 敲低降低了 總生存期CC 細(xì)胞的運(yùn)動性。此外，波形蛋白的免疫組織化學(xué)研究確定了波形蛋白表達(dá)與 Sam68 表達(dá)以及頸部淋巴結(jié)轉(zhuǎn)移之間的關(guān)聯(lián)?？傊狙芯勘砻?，Sam68 的高表達(dá)可能通過調(diào)節(jié)波形蛋白表達(dá)和 總生存期CC 中的運(yùn)動間充質(zhì)表型促進(jìn)轉(zhuǎn)移。關(guān)鍵詞：有絲分裂中的 Src 相關(guān) 68 kDa；上皮間質(zhì)轉(zhuǎn)化；轉(zhuǎn)移;動力;口腔癌;波形蛋白

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

The present study aimed to investigate the clinical and biological significance of Src?associated in mitosis 68 kDa (Sam68) in oral squamous cell carcinoma (OSCC). Immunohistochemical analysis was performed on tissue samples obtained from 77 patients with OSCC. Univariate analysis revealed that the high expression of Sam68 was significantly correlated with advanced pathological T stage (P=0.01), positive lymphovascular invasion (P=0.01), and pathological cervical lymph node metastasis (P<0.01). Moreover, multivariate analysis demonstrated that the high expression of Sam68 was an independent predictive factor for cervical lymph node metastasis (odds ratio, 4.39; 95% confidence interval, 1.49?14.23; P<0.01). These results indicated that high Sam68 expression contributed to tumor progression, especially cervical lymph node metastasis, in OSCC. mRNA sequencing was also performed to assess the changes in the transcriptome between OSCC cells with Sam68 knockdown and control cells with the aim of elucidating the biological roles of Sam68. Gene Ontology enrichment analysis revealed that downregulated differentially expressed genes (DEGs) were concentrated in some biological processes related to epithelial?mesenchymal transition. Among these DEGs, it was established that vimentin was particularly downregulated in these cells. It was also confirmed that Sam68 knockdown reduced the motility of OSCC cells. Furthermore, the immunohistochemical study of vimentin identified the association between vimentin expression and Sam68 expression as well as cervical lymph node metastasis. In conclusion, the present study suggested that the high expression of Sam68 may contribute to metastasis by regulating vimentin expression and a motile mesenchymal phenotype in OSCC.Keywords:?Src?associated in mitosis 68?kDa; epithelial?mesenchymal transition; metastasis; motility; oral cancer; vimentin