【佳學基因檢測】SHMT2 誘導頭頸癌的干性和進展

基因檢測—實操性

數(shù)據(jù)分析《腫瘤治療效果與基因檢測結果的相關性》《Int J Mol Sci》在.?2022 Aug 26;23(17):9714.發(fā)表了一篇題目為《SHMT2 誘導頭頸癌的干性和進展》腫瘤靶向藥物治療基因檢測臨床研究文章。該研究由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)容關鍵詞：

SHMT2,癌癥干細胞,頭頸癌,進展

腫瘤靶向治療基因檢測臨床應用結果

一碳代謝途徑中的各種酶與腫瘤的發(fā)生發(fā)展密切相關，都可以成為癌癥治療的潛在靶點。絲氨酸羥甲基轉移酶2（SHMT2）是一種關鍵的代謝酶，對癌細胞的增殖和生長非常重要。然而，SHMT2在頭頸癌（HNC）中的作用和機制尚不清楚。癌癥基因組圖譜（TCGA）數(shù)據(jù)分析顯示，SHMT2在腫瘤組織中的表達高于正常組織，其表達與男性、侵襲性組織學分級、淋巴結轉移、遠處轉移、晚期TNM顯著相關。 HNC的分期和淋巴血管侵犯。 FADU 和 SNU1041 細胞系中的 SHMT2 敲低顯著抑制了細胞增殖、集落形成、遷移和侵襲。此外，使用 TCGA 數(shù)據(jù)進行的基因本體論 (GO) 和京都基因和基因組百科全書 (KEGG) 通路富集分析表明，SHMT2 與癌癥干細胞的調(diào)控和維持密切相關。此外，我們發(fā)現(xiàn)與對照組相比，沉默 SHMT2 抑制了干性標志物的表達和腫瘤球體的形成。相反，在HEP-2細胞中過表達SHMT2后，干性標志物顯著增加。有趣的是，我們發(fā)現(xiàn)敲除 SHMT2 會降低與 Notch 和 Wnt 通路相關的基因的表達。賊后，沉默 SHMT2 顯著降低了異種移植模型中的腫瘤生長和干細胞標記?？傊覀兊难芯勘砻靼邢?SHMT2 可能在抑制 HNC 進展中發(fā)揮重要作用。癌癥干細胞；頭頸癌；進展。

腫瘤發(fā)生與反復轉移國際數(shù)據(jù)庫描述：

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.