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背景与目的:近年来,多不饱和脂肪酸对肿瘤发生、发展影响的研究备受关注.本实验主要观察两种ω-3多不饱和脂肪酸(ω-3 polyunsaturated fatty acid,ω-3 PUFA)二十碳五烯酸(eicosapentaenoic acid,EPA)和二十二碳六烯酸(docosahexaenoic acid,DHA)对人前列腺癌细胞株PC-3转移的影响,并通过检测ω-3 PUFA对细胞内Rho GTP酶蛋白表达及细胞骨架重组影响,揭示Rho GTP酶在ω-3 PUFA抑制肿瘤转移中的作用.方法:MTT法观察ω-3 PUFA对PC-3细胞增殖能力的影响,体外粘附实验、侵袭实验和迁移实验观察ω-3 PUFA对肿瘤细胞转移的影响.Western blot法检测ω-3 PUFA对与细胞骨架重组相关的RhoA、Rac1、Rac2和Cdc42蛋白表达的影响.免疫荧光细胞化学法标记微丝和微管,激光共聚焦扫描显微镜观察ω-3 PUFA对细胞骨架重组的影响.结果:EPA及DHA均能抑制PC-3细胞增殖,增殖抑制率均随处理浓度增大和作用时间延长而增加.与对照组比较,60μmol/L的EPA或DHA处理后的PC-3细胞体外粘附性、侵袭性和迁移性均显著下降(P<0.05).ω-3 PUFA能显著下调Rac1、Rac2和Cdc42蛋白表达(P<0.05),并能明显影响细胞内微丝和微管细胞骨架的结构和分布.结论:ω-3 PUFA能够通过下调Rho GTP酶基因表达,抑制Rho GTP酶对细胞骨架重组的调控,导致细胞骨架结构改变,削弱肿瘤细胞的粘附性、侵袭性和迁移性,抑制PC-3细胞的转移. 相似文献
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信号转导与转录激活因子(STAT3)可被多种细胞因子激活,参与肿瘤细胞增殖、血管生成、肿瘤侵袭和化疗耐药等过程.上皮-间质转化(EMT)在肿瘤的侵袭转移及化疗耐药等过程中也起重要作用.研究表明,STAT3可通过调控EMT,改变肿瘤的侵袭转移能力,增强肿瘤细胞对化疗药物的耐药性.探讨STAT3与EMT在肿瘤细胞中的作用及其相互关系有助于为分子靶向治疗提供可靠的理论依据. 相似文献
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目的:总结白细胞介素-18(IL-18)与肿瘤的侵袭、转移之间关系的研究现状,探讨其在肿瘤侵袭、转移中的重要作用机制.方法:应用PubMed及CNKI期刊全文数据库检索系统,以“IL-18,白细胞介素-18,肿瘤”等为关键词,检索2005-01-01—2012-03-31相关文献,共检到文献680条.纳入标准:1)IL-18促进肿瘤侵袭、转移的机制;2)IL-18抑制肿瘤侵袭、转移的机制;3)IL-18在不同肿瘤中的异常表达与预后.根据纳入标准符合分析的文献41篇.结果:IL 18主要通过免疫调节、影响肿瘤血管生成和对细胞因子及其受体的调节等多种复杂机制来实现对肿瘤生物学行为的介入.当IL-18表现为免疫激活或是抑制肿瘤血管生成活性时,主要发挥其抑制肿瘤的作用;当IL-18在免疫逃逸、细胞外基质降解、肿瘤细胞黏附和肿瘤血管生成等方面表现为促进作用时,其亲肿瘤效应尤为显著.但是IL-18在不同肿瘤中上调或下调的具体机制尚不清楚.IL-18与VEGF、黏附分子、趋化因子、M-CSF、TNF和MMPs等其他肿瘤侵袭转移相关因子间的关系及信号转导机制也需进一步完善.结论:IL-18在肿瘤侵袭转移中的作用具有两面性,其具体的调控机制和作用条件需要更加深入地研究和综合分析. 相似文献
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目的:探讨不饱和脂肪酸ω-3、ω-6及中间代谢产物(PEG2、PEG3)对胃癌细胞侵袭势能的影响,分析ω-3和ω-6对胃癌转移的分子生物学机制.方法:RT-PCR检测COX-1和COX-2在胃癌细胞中的表达水平;细胞侵袭实验分别检测ω-3、ω-6、PFG2和PEG3对胃癌细胞侵袭势能.结果:COX-2只表达于MKN74和MKN45细胞株中,而COX-1在4种胃癌细胞株中均有表达.在COX-2阳性表达的胃癌细胞株中,ω-6(AA)及PEG2能明显强化胃癌细胞的侵袭能力;ω-3(EPA)及PEG3能抑制胃癌细胞的侵袭.在COX-2阴性表达的胃癌细胞株中,ω-6(AA)及PEG2则对胃癌的侵袭能力无明显影响;ω-3 (EPA)及PEG3则能明显抑制胃癌细胞的侵袭.COX-2阳性细胞株中抑制COX-2活性后,ω-6 (AA)+ PEG2对胃癌细胞的侵袭能力无明显改变.结论:ω-6不饱和脂肪酸能够强化胃癌细胞的侵袭能力;ω-3不饱和脂肪酸能明显抑制胃癌细胞的侵袭能力;ω-6不饱和脂肪酸与COX-2结合后生成PGE2强化胃癌细胞的侵袭能力;ω-3和COX-1结合后生成PGE3抑制胃癌细胞的侵袭能力. 相似文献
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CD44与肿瘤的免疫逃逸 总被引:4,自引:0,他引:4
CD44在多种肿瘤细胞表达上调或发生构型改变,通过多种机制参与远处侵袭转移.最新研究表明,CD44在肿瘤免疫逃逸中发挥重要作用,通过诱导肿瘤细胞Fas表达异常、抵抗凋亡及构型改变等多种机制参与肿瘤的免疫逃逸. 相似文献
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肝细胞癌(hepatocellular carcinoma,HCC)是我国常见的恶性肿瘤。转移、扩散是其预后不良的主要原因。因此,探索肿瘤发生、发展和侵袭转移的分子机制,寻求新的治疗靶点,对于提高肝癌的疗效具有重要意义。microRNA简称为miRNA,通常长度为19-25个核苷酸,广泛存在于真核生物中,是一类高度保守的非编码的小分子单链RNA。miRNA通过与靶mRNA3’-UTR区完全或部分互补结合,导致靶区降解或转录后翻译抑制,从而调控靶基因的表达。miRNA具有癌基因和抑癌基因的作用,直接或间接参与肝癌发生和发展。 相似文献
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Mexidol therapy inhibited cyclophosphamide-induced myelosuppression in C57B1/6 line mice with Lewis lung carcinoma without affecting antitumor action of the latter. Mexidol plus cyclophosphamide proved more effective in prophylaxis of metastasis as compared with the cytostatic alone. 相似文献
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S Tsuru M Togami M Taniguchi K Nomoto 《Gan to kagaku ryoho. Cancer & chemotherapy》1988,15(6):1915-1920
An experimental model is introduced for the study on liver metastasis using intrasplenically injected EL-4 and Lewis lung tumor (LLT) cells. The inhibitory effects of UFT, FT and 5-FU on the frequencies of metastatic foci in the liver were compared. All drugs showed inhibitory effect on the frequencies of liver metastasis. However, a high dose of UFT suppressed strongly the frequencies of liver metastasis. In order to compare the immunosuppressive activity of UFT with that of FT and 5-FU at the dose to give 50% inhibition of liver metastasis (MED50), we determined the MED50 values of UFT, FT or 5-FU against liver metastasis of EL-4 and LLT cells. FT and 5-FU were suppressed strongly the humoral response against SRBC, the delayed hypersensitivity against picryl chloride and the phagocytic activity. UFT had no inhibitory effect on immune responses. 相似文献
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M Urano L A Kenton J Kahn 《International journal of radiation oncology, biology, physics》1988,15(1):159-166
The effect of hyperthermia on radiation-induced early- and late-appearing foot reactions was studied in C3Hf/Sed mice derived from our defined flora mouse colony. The animal foot was irradiated with 137Cs gamma-rays under hypoxic, air, or hyperbaric oxygen (O2 30 psi) conditions. Hyperthermia of 43.5 degrees C for 45 min was given locally in a water bath where a constant temperature +/- 0.1 degrees C was maintained. Treatment intervals between the 2 treatments were 20 min and 2 days. For the early-appearing reactions scores taken between the 14th and 35th post-irradiation days were averaged. Late-appearing reactions became apparent after approximately the 200th post-treatment day and increased with time. The foot reaction was enhanced by hyperthermia given 20 min before or after irradiation. Dose response curves for radiation given 20 min after hyperthermia for acute-appearing reactions lacked shoulders, whereas those following the same treatment schedule for late-appearing reactions showed significant shoulders. The thermal enhancement ratios (TER) for score 2.0 (complete epilation) early- and late-appearing reactions depended on the treatment interval and sequence. The TER values were greater for a short treatment interval (20 min.) than for a long treatment interval (2 days). Thermal enhancement was greater for hyperthermia given before irradiation compared to the reverse sequence. The TER values were always smaller for the late-appearing reactions than for the acute-appearing reactions. The relationships between early reaction scores and late reaction scores showed that the late reactions following combined heat and radiation are less extensive than those following radiation alone if they were compared at radiation doses which induced an equal level of early reactions. This difference was most significant at low early reaction scores and decreased with increasing score level. 相似文献
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血栓素A2,前列环素与Lewis肺癌生长及转移关系的实验研究 总被引:2,自引:0,他引:2
实验观察了血栓素A2、前列环素与Lewis肺癌生长及转移的关系,证实肿瘤肺部转移灶数目与血栓素A2呈正相关,与前列环素呈负相关,与血栓素A2/前列环素之比呈对数正相关;肿瘤大小与血栓素A2呈正相关,与前列环素呈抛物线相关。结果提示血栓素A2促进Lewis肺癌转移,前列环素抑制Lewis肺癌转移;Lewis肺癌主要表现为抑制前列环素合成,但在肿瘤早期,亦见促进前列环素合成现象。 相似文献
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目的:内皮抑素是一种特异性血管内皮生长抑制因子,本研究目的在于探讨人内皮抑素对卵巢癌SKOV3细胞生长的抑制作用及其机制。方法:MTT法观测内皮抑素对SKOV3细胞的生长抑制作用;透射电镜观察内皮抑素处理SKOV3细胞后细胞的凋亡情况,流式细胞仪检测细胞凋亡率及细胞周期;RT-PCR法检测内皮抑素处理SKOV3细胞后凋亡调控基因bcl-2和baxmRNA的表达。结果:内皮抑素具有体外抑制SK-OV3细胞增殖的作用,15μg/ml内皮抑素组的A490值(0.454)明显低于PBS对照组(0.686)(P〈0.01);内皮抑素能诱导SKOV3细胞凋亡;内皮抑素对SKOV3细胞中bcl-2和bax的表达无明显改变;结论:人内皮抑素具有抑制SKOV3细胞生长的作用,其机制可能与诱发细胞凋亡相关。 相似文献