【广东会GDH基因检测】SHMT2 诱导头颈癌的干性和进展
基因检测—实操性
数据分析《肿瘤治疗效果与基因检测结果的相关性》《Int J Mol Sci》在. 2022 Aug 26;23(17):9714.发表了一篇题目为《SHMT2 诱导头颈癌的干性和进展》肿瘤靶向药物治疗基因检测临床研究文章。该研究由Yanli Jin, Seung-Nam Jung, Mi Ae Lim, Chan Oh, Yudan Piao, Hae Jong Kim, QuocKhanh Nguyena, Yea Eun Kang, Jae Won Chang, Ho-Ryun Won, Bon Seok Koo等完成。促进了肿瘤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:
SHMT2,癌症干细胞,头颈癌,进展
肿瘤靶向治疗基因检测临床应用结果
一碳代谢途径中的各种酶与肿瘤的发生发展密切相关,都可以成为癌症治疗的潜在靶点。丝氨酸羟甲基转移酶2(SHMT2)是一种关键的代谢酶,对癌细胞的增殖和生长非常重要。然而,SHMT2在头颈癌(HNC)中的作用和机制尚不清楚。癌症基因组图谱(TCGA)数据分析显示,SHMT2在肿瘤组织中的表达高于正常组织,其表达与男性、侵袭性组织学分级、淋巴结转移、远处转移、晚期TNM显着相关。 HNC的分期和淋巴血管侵犯。 FADU 和 SNU1041 细胞系中的 SHMT2 敲低显着抑制了细胞增殖、集落形成、迁移和侵袭。此外,使用 TCGA 数据进行的基因本体论 (GO) 和京都基因和基因组百科全书 (KEGG) 通路富集分析表明,SHMT2 与癌症干细胞的调控和维持密切相关。此外,我们发现与对照组相比,沉默 SHMT2 抑制了干性标志物的表达和肿瘤球体的形成。相反,在HEP-2细胞中过表达SHMT2后,干性标志物显着增加。有趣的是,我们发现敲除 SHMT2 会降低与 Notch 和 Wnt 通路相关的基因的表达。贼后,沉默 SHMT2 显着降低了异种移植模型中的肿瘤生长和干细胞标记。总之,我们的研究表明靶向 SHMT2 可能在抑制 HNC 进展中发挥重要作用。癌症干细胞;头颈癌;进展。
肿瘤发生与反复转移国际数据库描述:
Various enzymes in the one-carbon metabolic pathway are closely related to the development of tumors, and they can all be potential targets for cancer therapy. Serine hydroxymethyltransferase2 (SHMT2), a key metabolic enzyme, is very important for the proliferation and growth of cancer cells. However, the function and mechanism of SHMT2 in head and neck cancer (HNC) are not clear. An analysis of The Cancer Genome Atlas (TCGA) data showed that the expression of SHMT2 was higher in tumor tissue than in normal tissue, and its expression was significantly associated with male sex, aggressive histological grade, lymph node metastasis, distant metastasis, advanced TNM stage, and lymphovascular invasion in HNC. SHMT2 knockdown in FADU and SNU1041 cell lines significantly inhibited cell proliferation, colony formation, migration, and invasion. Additionally, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses using TCGA data revealed that SHMT2 was closely related to cancer stem cell regulation and maintenance. Furthermore, we found that silencing SHMT2 inhibited the expression of stemness markers and tumor spheroid formation compared with a control group. On the contrary, stemness markers were significantly increased after SHMT2 overexpression in HEP-2 cells. Interestingly, we found that knocking down SHMT2 reduced the expression of genes related to the Notch and Wnt pathways. Finally, silencing SHMT2 significantly reduced tumor growth and decreased stemness markers in a xenograft model. Taken together, our study suggests that targeting SHMT2 may play an important role in inhibiting HNC progression.Keywords: SHMT2; cancer stemness; head and neck cancer; progression.
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