【佳學(xué)基因檢測】騰龍補中顆粒與結(jié)腸癌基因檢測

小孩發(fā)育遲緩查基因有用嗎排名

研究腫瘤基因檢測中的數(shù)據(jù)庫比對與基因解碼了解《J Tradit Chin Med》在. 2022 Oct;42(5):701-706.發(fā)表了一篇題目為《騰龍補中顆粒抑制SW620人結(jié)腸癌的生長》腫瘤靶向藥物治療基因檢測臨床研究文章。該研究由L I Miao, Zheng Jialu, Wang Shuangshuang, Chen Lei, Peng Xiao, Chen Jinfang, A N Hongmei, H U Bing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(guān)鍵詞：

騰龍補中顆粒,血管生成,細胞凋亡,細胞衰老,結(jié)腸腫瘤,信號轉(zhuǎn)導(dǎo)

腫瘤靶向治療基因檢測臨床應(yīng)用結(jié)果

目的：觀察騰龍補中湯顆粒制劑即騰龍補中顆粒（，TBG）對人SW620結(jié)腸癌的抗癌作用。用 TBG（2.56 g/kg，每天一次）和/或 5-Fu（104 mg/kg，每周一次）治療 21 天。通過商業(yè)試劑盒測量細胞凋亡、半胱天冬酶活性和細胞衰老。 Western blot或免疫組化檢測蛋白表達和磷酸化。結(jié)果：TBG和5-Fu抑制腫瘤生長。 TBG、5-Fu、TBG+5-Fu組的抑瘤率分別為42.25%、51.58%、76.08%。 TBG 和 5-Fu 的組合顯示出協(xié)同抗癌作用。 TBG 和 5-Fu 誘導(dǎo)細胞凋亡，激活 caspase-3、-8 和 -9，增加 SMAC 表達，抑制 XIAP 表達。 TBG 誘導(dǎo)細胞衰老，上調(diào)細胞周期蛋白依賴性激酶抑制劑 1a (CDKN1a) 和細胞周期蛋白依賴性激酶抑制劑 2a (CDKN2a) 的表達，并抑制視網(wǎng)膜母細胞瘤相關(guān)蛋白 (RB) 的磷酸化和細胞周期蛋白 E1 (CCNE1) 的表達和細胞周期蛋白依賴性2. TBG 還抑制血管生成，同時下調(diào)血管內(nèi)皮生長因子 (VEGF) 和缺氧誘導(dǎo)因子-1α (HIF-1α)。結(jié)論：TBG 抑制 SW620 結(jié)腸癌生長，誘導(dǎo)細胞凋亡 SMAC-XIAP-Caspase信號通路，通過CDKN1a/CDKN2a-RB-E2F信號通路誘導(dǎo)細胞衰老，通過下調(diào)HIF-1α和VEGF抑制血管生成，增強5-Fu的作用。血管生成；細胞凋亡；細胞衰老；結(jié)腸腫瘤；信號轉(zhuǎn)導(dǎo)。

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

Objective: To observe the anticancer effects of the granular preparation of Tenglong Buzhong decoction (,TBD), i.e Tenglong Buzhong granules (, TBG), in human SW620 colon cancer.Methods: BALB/c nude mice were subcutaneously transplanted with SW620 cells, and treated with TBG (2.56 g/kg, once per day) and/or 5-Fu (104 mg/kg, once per week) for 21 d. Apoptosis, Caspase activities and cellular senescence were measured by commercial kits. The protein expression and phosphorylation were detected by Western blot or immunohistochemistry.Results: TBG and 5-Fu inhibited tumor growth. The tumor inhibition rate of the TBG, 5-Fu, and TBG+5-Fu groups was 42.25%, 51.58%, and 76.08%, respectively. Combination of TBG and 5-Fu showed synergetic anti-cancer effects. TBG and 5-Fu induced apoptosis, activated caspase-3, -8, and -9, increased SMAC expression, inhibited XIAP expression. TBG induced cellular senescence, upregulated cyclin-dependent kinase inhibitor 1a (CDKN1a) and cyclin-dependent kinase inhibitor 2a (CDKN2a) expression, and inhibited phosphorylation of retinoblastoma-associated protein (RB) and expression of cyclin E1 (CCNE1) and cyclin-dependent kinases (CDK) 2. TBG also inhibited angiogenesis accompanied by downregulation of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor-1α (HIF-1α).Conclusions: TBG inhibits SW620 colon cancer growth, induces apoptosis SMAC-XIAP-Caspases signaling, induces cellular senescence through CDKN1a/CDKN2a-RB-E2F signaling, inhibits angiogenesis by down-regulation of HIF-1α and VEGF, and enhances the effects of 5-Fu.Keywords: Tenglong Buzhong granules; angiogenesis; apoptosis; cellular senescence; colonic neoplasms; signal transduction.