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81.
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为了探讨miR-200b在辐射诱导胸腺淋巴瘤中的作用与机制,采用全身分割照射建立BALB/c小鼠辐射诱导胸腺淋巴瘤模型,检测miR-200b表达情况;构建过表达与敲低miR-200b细胞模型,检测该miRNA对细胞增殖、凋亡情况的影响;随后通过miRNA数据库TargetScan分析miRNA潜在靶点,并用双荧光素酶报告系统进行验证,最后采用Spearman方法分析TBK1蛋白与miR-200b表达水平的相关性。结果显示,小鼠辐射诱导胸腺淋巴瘤组织中miR-200b表达下调,过表达miR-200b可明显抑制细胞增殖,增加细胞凋亡,下调miR-200b可促进细胞增殖,减少细胞凋亡;双荧光素酶报告系统提示miR-200b以3' UTR依赖的方式靶向作用于TBK1。在辐射诱导胸腺淋巴瘤样本中,miR-200b表达和TBK1蛋白水平之间存在负相关关系,且TBK1过表达可部分逆转miR-200b介导的细胞生物学效应。结果表明,辐射诱导胸腺淋巴瘤组织中miR-200b表达下调,其直接靶点TBK1表达上调;过表达miR-200b可明显抑制胸腺淋巴瘤细胞增殖,增加细胞凋亡。提示靶向调控miR-200b/TBK1,有望成为防治辐射诱导胸腺淋巴瘤的潜在新途径。 相似文献
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A concise, convergent synthesis of 11,12-dimethoxydibenzo[def,p]chrysene (5), a preferred precursor for the synthesis of the carcinogenic metabolites of a highly potent carcinogen dibenzo[def,p]chrysene (DBC, 1) has been described. Suzuki cross-coupling reaction of 5,5-dimethyl-2-(3,4-dimethoxy-2-formyl)-1,3,2-dioxaborinane (6a) with 7-bromo-5,6-dihydro-4H-benz[de]anthracene (7) afforded 7-(2-formyl-3,4-dimethoxyphenyl)- 5,6-dihydro-4H-benz[de]anthracene (9). Treatment of 9 with an excess of potassium tert-butoxide produced 11,12-dimethoxydibenzo[def,p]chrysene (5) in overall 51% yield based on 6a. 相似文献
86.
介绍了 2 0 0 0年 5月 1 7日在日本广岛举行的“从生物学观点探讨辐射防护政策的新思路”研讨会上 ,由 D.Preston,Y.Ishikawa,P.Duport,C.Streffer,M.Ohtaki,M.N.Mohankumar和 X.A.Chen等 7位专家所作的发言 ,内容包括 :广岛和长崎原子弹爆炸幸存者的辐射效应 ;二氧化钍造影剂病人肝和肺的致癌 ;受到低剂量电离辐射照射的动物的癌的危险 ;辐射诱发癌的致癌机制 ;把诱发遗传不稳定性假说作为依据的辐射致癌的数学含义 ;对电离辐射的适应性响应及其在影响放射防护标准中的作用以及长期吸入钍尘对健康影响的 1 4年追踪。 相似文献
87.
Mayes Alswady-Hoff Johanna Samulin Erdem Santosh Phuyal Oskar Knittelfelder Animesh Sharma Davi de Miranda Fonseca
ivind Skare Geir Slupphaug Shanbeh Zienolddiny 《International journal of molecular sciences》2021,22(10)
There is little in vitro data available on long-term effects of TiO2 exposure. Such data are important for improving the understanding of underlying mechanisms of adverse health effects of TiO2. Here, we exposed pulmonary epithelial cells to two doses (0.96 and 1.92 µg/cm2) of TiO2 for 13 weeks and effects on cell cycle and cell death mechanisms, i.e., apoptosis and autophagy were determined after 4, 8 and 13 weeks of exposure. Changes in telomere length, cellular protein levels and lipid classes were also analyzed at 13 weeks of exposure. We observed that the TiO2 exposure increased the fraction of cells in G1-phase and reduced the fraction of cells in G2-phase, which was accompanied by an increase in the fraction of late apoptotic/necrotic cells. This corresponded with an induced expression of key apoptotic proteins i.e., BAD and BAX, and an accumulation of several lipid classes involved in cellular stress and apoptosis. These findings were further supported by quantitative proteome profiling data showing an increase in proteins involved in cell stress and genomic maintenance pathways following TiO2 exposure. Altogether, we suggest that cell stress response and cell death pathways may be important molecular events in long-term health effects of TiO2. 相似文献
88.
Elisabetta Rubini Marco Minacori Giuliano Paglia Fabio Altieri Silvia Chichiarelli Donatella Romaniello Margherita Eufemi 《International journal of molecular sciences》2021,22(11)
Organochlorine pesticides constitute the majority of the total environmental pollutants, and a wide range of compounds have been found to be carcinogenic to humans. Among all, growing interest has been focused on β-hexachlorocyclohexane (β-HCH), virtually the most hazardous and, at the same time, the most poorly investigated member of the hexachlorocyclohexane family. Considering the multifaceted biochemical activities of β-HCH, already established in our previous studies, the aim of this work is to assess whether β-HCH could also trigger cellular malignant transformation toward cancer development. For this purpose, experiments were performed on the human normal bronchial epithelium cell line BEAS-2B exposed to 10 µM β-HCH. The obtained results strongly support the carcinogenic potential of β-HCH, which is achieved through both non-genotoxic (activation of oncogenic signaling pathways and proliferative activity) and indirect genotoxic (ROS production and DNA damage) mechanisms that significantly affect cellular macroscopic characteristics and functions such as cell morphology, cell cycle profile, and apoptosis. Taking all these elements into account, the presented study provides important elements to further characterize β-HCH, which appears to be a full-fledged carcinogenic agent. 相似文献
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Alina Florentina Vladu Denisa Ficai Alexandra Gabriela Ene Anton Ficai 《International journal of molecular sciences》2022,23(18)
Polyphenols represent a structural class of mainly natural organic chemicals that contain multiple phenol structural units. The beneficial properties of polyphenols have been extensively studied for their antitumor, anti-inflammatory, and antibacterial effects, but nowadays, their medical applications are starting to be extended to many other applications due to their prebiotic role and their impact on the microbiota. This review focused on the use of polyphenols in cancer treatment. Their antineoplastic effects have been demonstrated in various studies when they were tested on numerous cancer lines and some in in vivo models. A431 and SCC13 human skin cancer cell lines treated with EGCG presented a reduced cell viability and enhanced cell death due to the inactivation of β-catenin signaling. Additionally, resveratrol showed a great potential against breast cancer mainly due to its ability to exert both anti-estrogenic and estrogenic effects (based on the concentration) and because it has a high affinity for estrogen receptors ERα and Erβ. Polyphenols can be combined with different classical cytostatic agents to enhance their therapeutic effects on cancer cells and to also protect healthy cells from the aggressiveness of antitumor drugs due to their anti-inflammatory properties. For instance, curcumin has been reported to reduce the gastrointestinal toxicity associated with chemotherapy. In the case of 5-FU-induced, it reduced the gastrointestinal toxicity by increasing the intestinal permeability and inhibiting mucosal damage. Co-administration of EGCG and doxorubicin induced the death of liver cancer cells. EGCG has the ability to inhibit autophagic activity and stop hepatoma Hep3B cell proliferation This symbiotic approach is well-known in medical practice including in multiple chemotherapy. 相似文献