【佳学基因检测】Sam68的高表达通过调节波形蛋白表达和口腔鳞状细胞癌的运动表型促进转移

基因突变癫疯病会好吗排队

分析基因检测与基因解码的区别与选择体会到《Oncol Rep》在. 2022 Oct;48(4):183.发表了一篇题目为《Sam68的高表达通过调节波形蛋白表达和口腔鳞状细胞癌的运动表型促进转移》dota2吧雷电竞 dota2吧雷电竞 治疗基因检测临床研究文章。该研究由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。促进了dota2吧雷电竞 的正确治疗与个性化用药的发展，进一步强调了基因信息检测与分析的重要性。

肿瘤靶向药物及正确治疗临床研究内容关键词：

Src 相关的有丝分裂 68 kDa,上皮间质转化,转移,动力,口腔癌,波形蛋白

肿瘤靶向治疗基因检测临床应用结果

本研究旨在探讨 Src 相关的有丝分裂 68 kDa (Sam68) 在口腔鳞状细胞癌 (总生存期CC) 中的临床和生物学意义。对从 77 名 总生存期CC 患者获得的组织样本进行免疫组织化学分析。单因素分析显示，Sam68的高表达与晚期病理T分期（P=0.01）、阳性淋巴血管浸润（P=0.01）、病理性颈淋巴结转移（P<0.01）显着相关。此外，多因素分析表明，Sam68 的高表达是颈部淋巴结转移的独立预测因素（优势比，4.39；95% 置信区间，1.49-14.23；P<0.01）。这些结果表明，Sam68 的高表达有助于 总生存期CC 中的肿瘤进展，尤其是颈部淋巴结转移。还进行了 mRNA 测序以评估具有 Sam68 敲低的 总生存期CC 细胞和对照细胞之间转录组的变化，目的是阐明 Sam68 的生物学作用。基因本体富集分析表明，下调的差异表达基因（DEGs）集中在一些与上皮-间质转化相关的生物学过程中。在这些 DEG 中，确定波形蛋白在这些细胞中特别下调。还证实 Sam68 敲低降低了 总生存期CC 细胞的运动性。此外，波形蛋白的免疫组织化学研究确定了波形蛋白表达与 Sam68 表达以及颈部淋巴结转移之间的关联。总之，本研究表明，Sam68 的高表达可能通过调节波形蛋白表达和 总生存期CC 中的运动间充质表型促进转移。关键词：有丝分裂中的 Src 相关 68 kDa；上皮间质转化；转移;动力;口腔癌;波形蛋白

肿瘤发生与反复转移国际数据库描述：

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