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| 1 | Hepatocellular carcinoma: Mechanisms of progression and immunotherapy显示文摘Liver cancer is one of the most common malignancies,and various pathogenic factors can lead to its occurrence and development.Among all primary liver cancers,hepatocellular carcinoma(HCC)is the most common.With extensive studies,an increasing number of molecular mechanisms that promote HCC are being discovered.Surgical resection is still the most effective treatment for patients with early HCC.However,early detection and treatment are difficult for most HCC patients,and the postoperative recurrence rate is high,resulting in poor clinical prognosis of HCC.Although immunotherapy takes longer than conventional chemotherapy to produce therapeutic effects,it persists for longer.In recent years,the emergence of many new immunotherapies,such as immune checkpoint blockade and chimeric antigen receptor T cell therapies,has given new hope for the treatment of HCC. | Yu Jiang Qiu-Ju Han Jian Zhang | 2019 | World Journal of Gastroenterology2019，25，25： | 21 |
| 2 | HMBOX1 negatively regulates NK cell functions by suppressing the NKG2D/DAP10 signaling pathway显示文摘HMBOX1 is a new member of the homeobox family.Homeobox members have been reported to participate in embryonic development and systemic metabolism,but the function of HMBOX1 remains unclear,especially in the hematopoietic system.Here,we show that HMBOX1is expressed at a high level in primary humanNKcells but is expressed at much lower levels inNKcell lines.Overexpression of HMBOX1 significantly inhibited NK cell activities,including natural cytotoxicity against tumor cells,the level of CD107a(a marker protein for degranulation)and the production of cytolytic proteins(perforin and granzymes).More interestingly,HMBOX1 negatively regulated the expression of NKG2D and the activation of the NKG2D/DAP10 signaling pathway in NK cells.This effect was reversed by knocking down HMBOX1.Taken together,these findings demonstrate that HMBOX1 may act as a negative regulator of NK cell functions via suppressing the NKG2D/DAP10 signaling pathway. | Longyan Wu Cai Zhang Jian Zhang | 2011 | Cellular & Molecular Immunology2011，8，5： | 10 |
| 3 | miR-195-5p靶向HMBOX1调控胃癌细胞增殖迁移侵袭及凋亡的机制显示文摘目的探讨miR-195-5p在胃癌细胞增殖、迁移、侵袭及凋亡中的作用与机制。方法运用qRT-PCR法检测正常胃上皮细胞(GES)-1、胃癌细胞N87、SGC-7901、HGC-27中miR-195-5p、含有1的同源框(HMBOX1)的表达;将miR-NC组(转染miR-NC)、miR-195-5p组(转染miR-195-5p mimics)、si-NC组(转染si-NC)、si-HMBOX1组(转染si-HMBOX1)、miR-195-5p+pcDNA组(共转染miR-195-5p mimics和pcDNA)、miR-195-5p+pcDNA-HMBOX1组(共转染miR-195-5p mimics和pcDNA-HMBOX1)转染至HGC-27;Western印迹检测细胞中HMBOX1、survivin、基质金属蛋白酶(MMP)2、MMP9、B细胞淋巴瘤(Bcl)-2的蛋白表达;噻唑蓝(MTT)法检测细胞增殖;Transwell法检测细胞迁移侵袭;流式细胞术检测细胞凋亡;双荧光素酶报告基因检测实验检测细胞荧光活性。结果相比于正常胃上皮GES-1细胞,胃癌细胞N87、SGC-7901、HGC-27中miR-195-5p表达显著降低,HMBOX1表达显著升高;过表达miR-195-5p或敲减HMBOX1均可抑制HGC-27细胞增殖、迁移侵袭及促凋亡,下调survivin、MMP2、MMP9、Bcl-2,上调P21、Bcl-2相关X蛋白(Bax);miR-195-5p可靶向HMBOX1;过表达HMBOX1可恢复miR-195-5p对胃癌细胞的作用。结论miR-195-5p能抑制胃癌细胞的增殖、迁移和侵袭,并诱导细胞凋亡,机制与靶向HMBOX1相关,将可为胃癌的诊断及治疗提供依据。 | 田由京 张浩 陈兴超 李军 李合 | 2020 | 中国老年学杂志2020，40，15： | 2 |
| 4 | 核转录因子HMBOX1对肝癌细胞生物学特征的影响显示文摘目的:比较肝癌细胞系与肝细胞系中HMBOX1的表达水平,探讨其在肝癌发生、发展中的作用。方法:RT-PCR检测HMBOX1在多种肝癌细胞系和正常肝细胞系中的表达。利用分子生物学方法构建pEGFP:HMBOX1融合表达载体,采用脂质体方法转染HepG2肝癌细胞系,MTT方法及流式细胞技术评价转染后细胞增殖和细胞周期的变化。基因芯片技术分析表达载体转染HepG2后肿瘤相关信号通路的变化。结果:PCR结果显示肝癌细胞系HMBOX1 mRNA表达水平明显低于正常肝细胞系;pEGFP:HMBOX1融合表达载体转染HepG2后,细胞的增殖能力和周期未出现显著变化;基因芯片的结果提示转染表达载体的HepG2细胞,肿瘤和免疫信号通路相关基因的表达发生显著变化。结论:HMBOX1在多种肝癌细胞系表达下调,可能参与了多条与肿瘤和免疫相关信号通路的调节,为进一步阐明肝癌的发生机制提供了新的实验依据。 | 贾慧峰 陆楠 张建 | 2012 | 中国免疫学杂志2012，28，7： | 1 |
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