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| 1 | Silencing MYH9 blocks HBx-induced GSK3βubiquitination and degradation to inhibit tumor stemness in hepatocellular carcinoma显示文摘MYH9 has dual functions in tumors.However,its role in inducing tumor stemness in hepatocellular carcinoma(HCC)is not yet determined.Here,we found that MYH9 is an effective promoter of tumor stemness that facilitates hepatocellular carcinoma pathogenesis.Importantly,targeting MYH9 remarkably improved the survival of hepatocellular carcinoma-bearing mice and promoted sorafenib sensitivity of hepatocellular carcinoma cells in vivo.Mechanistic analysis suggested that MYH9 interacted with GSK3βand reduced its protein expression by ubiquitin-mediated degradation,which therefore dysregulated theβ-catenin destruction complex and induced the downstream tumor stemness phenotype,epithelial–mesenchymal transition,and c-Jun signaling in HCC.C-Jun transcriptionally stimulated MYH9 expression and formed an MYH9/GSK3β/β-catenin/c-Jun feedback loop.X protein is a hepatitis B virus(HBV)-encoded key oncogenic protein that promotes HCC pathogenesis.Interestingly,we observed that HBV X protein(HBX)interacted with MYH9 and induced its expression by modulating GSK3β/β-catenin/c-Jun signaling.Targeting MYH9 blocked HBX-induced GSK3βubiquitination to activate theβ-catenin destruction complex and suppressed cancer stemness and EMT.Based on TCGA database analysis,MYH9 was found to be elevated and conferred poor prognosis for hepatocellular carcinoma patients.In clinical samples,high MYH9 expression levels predicted poor prognosis of hepatocellular carcinoma patients.These findings identify the suppression of MYH9 as an alternative approach for the effective eradication of CSC properties to inhibit cancer migration,invasion,growth,and sorafenib resistance in HCC patients.Our study demonstrated that MYH9 is a crucial therapeutic target in HCC. | Xian Lin Ai-min Li Yong-Hao Li Rong-Cheng Luo Yu-Jiao Zou Yi-Yi Liu Chen Liu Ying-Ying Xie Shi Zuo Zhan Liu Zhen Liu Wei-Yi Fang | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 6 |
| 2 | miR-142-3p靶向调控RHOBTB3基因对肺癌A549细胞增殖能力的影响显示文摘目的观察肺癌组织miR-142-3p表达变化,探讨miR-142-3p靶向调控Rho相关结构域BTB蛋白质3(Rho-related BTB domain-containing protein 3,RHOBTB3)基因对肺癌A549细胞增殖能力的影响。方法肺癌患者35例,均行手术治疗,取手术切除癌组织及癌旁组织,采用实时荧光定量PCR法检测miR-142-3p及RHOBTB3 mRNA相对表达量。将对数生长期A549细胞分为miR-142-3p组和对照组,分别转染表达miR-142-3p的慢病毒和阴性对照慢病毒,转染48 h时采用实时荧光定量PCR法检测miR-142-3p相对表达量。筛选出稳定转染的miR-142-3p组A549细胞分为稳转miR-142-3p组和miR-142-3p+RHOBTB3组,稳定转染的对照组A549细胞分为稳转对照组和RHOBTB3组,miR-142-3p+RHOBTB3组、RHOBTB3组采用脂质体转染法转染表达RHOBTB3的质粒,稳转miR-142-3p组、稳转对照组不做处理。转染48 h, 4组采用Western blot法检测RHOBTB3蛋白相对表达量,采用CCK-8法检测培养96 h时细胞增殖率,采用细胞克隆形成实验检测细胞克隆形成数目。采用荧光素酶报告基因实验验证miR-142-3p靶向结合RHOBTB3基因。结果肺癌组织miR-142-3p相对表达量(0.58±0.27)低于癌旁组织(1.06±0.34)(t=-6.508,P<0.001),RHOBTB3 mRNA相对表达量(1.24±0.32)高于癌旁组织(0.51±0.29)(t=10.020,P<0.001)。miR-142-3p组细胞miR-142-3p相对表达量(9.45±1.80)高于对照组(1.05±0.32)(t=11.240,P<0.001)。稳转miR-142-3p组RHOBTB3蛋白相对表达量(0.47±0.05)、细胞增殖率[(48.56±9.97)%]及细胞克隆形成数目[(47.00±8.39)个]均低于稳转对照组[0.79±0.07、(100.00±8.71)%、(165.67±13.92)个]和miR-142-3p+RHOBTB3组[0.77±0.06、(95.82±9.79)%、(141.33±12.88)个](P<0.05),RHOBTB3组RHOBTB3蛋白相对表达量(1.20±0.12)、细胞增殖率[(153.23±18.29)%]及细胞克隆形成数目[(267.83±23.25)个]均高于miR-142-3p+RHOBTB3组(P<0.05)。荧光素酶报告基因实验结果显示,miR-142-3p+pMIR WT组荧光素酶活性(0.41±0.05)低于NC+pMIR WT组(1.01±0.12)(t=11.220,P<0.001),miR-142-3p+pMIRMUT组荧光素酶活性(0.95±0.09)与NC+pMIRMUT组(1.02±0.09)比较差异无统计学意义(t=1.322,P=0.216)。结论肺癌组织miR-142-3p表达下调、RHOBTB3表达上调,miR-142-3p可靶向RHOBTB3基因抑制肺癌A549细胞增殖。 | 万启飞 朱晓明 李基伟 姚文健 魏立 | 2022 | 中华实用诊断与治疗杂志2022，36，3： | 1 |
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