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目的:探讨肝星状细胞条件培养基(hepatic stellate cell conditioned medium,HSC-CM)对人肝癌PLC/PRF/5细胞耐药性的影响及其可能的机制。 方法: 用无血清RPMI 1640培养肝星状细胞LX-2,使其在缺营养的环境下活化,收集其条件培养上清即为HSC-CM。PLC/PRF/5细胞在HSC-CM条件下培养24 h后,顺铂处理12 h或24 h,采用流式细胞术检测PLC/PRF/5细胞的凋亡情况,MTT法检测PLC/PRF/5细胞的增殖,real-time PCR检测PLC/PRF/5细胞上皮间质转化(epithelial mesenchymal transition,EMT)相关基因的表达水平。 结果: 顺铂组12和24 h两个时间点PLC/PRF/5细胞的凋亡率为(22.34±1.12)%和(26.78±1.56)%;HSC-CM+顺铂组细胞的凋亡率为(17.22±1.42)%和(21.52±1.76)%,顺铂组细胞凋亡率显著高于HSC-CM+顺铂组(P<0.05)。同在这两个时间点,顺铂组和HSC-CM+顺铂组PLC/PRF/5细胞的增殖活性分别为(68.65±2.56)%和(79.47±1.43)%,(46.54±3.65)%和(62.77±2.89)%,HSC-CM+顺铂组细胞增殖活性均高于顺铂组(P<0.05)。Real-time PCR 结果显示,与顺铂组相比较,HSC-CM+顺铂组PLC/PRF/5细胞中上皮标记物钙黏蛋白(E-cadherin)的表达下降(P<0.05),而间质细胞标记物神经黏附素(N-cadherin)、波形蛋白(vimentin)以及EMT相关转录因 子Snail和ZEB1的表达显著上调(P<0.01)。 结论: HSC-CM可能通过诱导PLC/PRF/5细胞发生EMT,从而增强PLC/PRF/5 细胞对顺铂的抵抗作用。  相似文献   
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Background:

The purpose of this study was to characterise the oncogenic roles of C35, a novel protein binding partner of ΔNp73, in ovarian cancer and to investigate the functional significance of C35–ΔNp73 interaction in the regulation of chemo-resistance.

Methods:

C35 expression was evaluated by quantitative real-time PCR in human ovarian cancer tissues and cell lines. The aggressiveness of ovarian cancer cells overexpressing C35 was examined by cell proliferation, migration, soft agar and nude mouse xenograft. The significance of C35–ΔNp73 interaction in chemo-resistance was evaluated by apoptosis assays and cell viability after cisplatin treatment.

Results:

The expression of C35 was significantly enhanced in human ovarian cancer tissues. Overexpression of C35 augmented proliferation, migration and tumourigenicity in ovarian cancer cell lines. C35 knockdown inhibited cell motility and cell growth. The co-expression of C35 and ΔNp73 by transient or stable transfection in ovarian cancer cells induced greater resistance to cisplatin treatment than did transfection with C35 or ΔNp73 alone. The cisplatin resistance was demonstrated to be caused by increased AKT and NFκB activity induced by C35–ΔNp73.

Conclusion:

Our results suggest that ΔNp73 might cooperate with C35 to promote tumour progression and contribute to cisplatin resistance in ovarian cancer cells. Future studies of the functional roles of ΔNp73 and C35 will provide insight that will aid in the establishment of new strategies and more effective therapies.  相似文献   
4.
Recent studies have identified that constitutively active phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling is an important feature of osteosarcoma, where it promotes cell proliferation, survival, and chemo-resistance. Here, we studied the therapeutic potential of NVP-BEZ235, a novel dual PI3K/mTOR dual inhibitor, on osteosarcoma cells in vivo and in vitro. NVP-BEZ235 was cytotoxic and cytostatic to a panel of osteosarcoma lines (MG-63, U2OS and SaOs-2), where it induce apoptosis and cell-cycle arrest. At the molecular level, NVP-BEZ235 inhibited PI3K-AKT-mTORC1 activation and downregulated cyclin D1/cyclin B1 expressions, while increasing MEK/Erk phosphorylation in osteosarcoma cells. MEK/Erk inhibitors PD98059 and MEK-162 increased NVP-BEZ235 activity on osteosarcoma cells. In vivo, oral NVP-BEZ235 inhibited U2OS xenograft in SCID mice, and its anti-tumor efficiency was further enhanced by MEK-162 co-administration. Taken together, our findings indicate that dual inhibition of PI3K and mTOR with NVP-BEZ235, either alone or in combination with MEK/Erk inhibitors, may be an efficient treatment for osteosarcoma.  相似文献   
5.
The objective of this study was to characterize the oncogenic actions of a recently identified cancer-associated gene YWHAZ (also named as 14-3-3 ζ/δ) in urothelial carcinomas of the urinary bladder (UCUB). A genome-wide study revealed YWHAZ to be involved in the amplicon at 8q22.3, and its genetic amplification was detected predominantly in muscle-invasive bladder cancer (MIBC). Immunohistochemical staining confirmed the association of YWHAZ overexpression with higher tumor stages, lymph node/vascular invasion, and mitotic activity. Univariate and multivariate analyses further indicated the prognostic potential of YWHAZ for more aggressive cancer types. Both gene set enrichment analysis and STRING network studies suggested involvement of YWHAZ in regulating caspase-mediated apoptosis. Ectopic expression of YWHAZ in bladder cells with low endogenous YWHAZ levels boosted cell resistance to doxorubicin and cisplatin, as well as to ionizing radiation. Conversely, YWHAZ-knockdown using specific shRNA in cells with high endogenous YWHAZ levels diminished survival activity, suppressing cell growth and increasing cell death. Our findings confirm the essential role played by YWHAZ in sustaining cell proliferation during chemo/radiotherapy. Treatments based on anti-YWHAZ strategies may thus be beneficial for UCUB patients overexpressing YWHAZ. © 2019 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.  相似文献   
6.

Background:

Cancer stem cells (CSCs) are responsible for treatment failure. However, their identification and roles in resistance are not well established in head and neck squamous cell carcinoma (HNSCC).

Methods:

Three HNSCC cell lines (FaDu, Detroit562 and BICR6) were treated with cisplatin or radiation. Cell surface antigens were analysed by LyoPlate, a novel cell surface antigen array. The expression levels of antigens highly expressed after treatments were further compared between cisplatin-resistant Detroit562 cells and its parental line. Association of the candidate antigen with CSCs properties, namely sphere formation and in vivo tumourigenicity, was also examined.

Results:

CD10, CD15s, CD146 and CD282 were upregulated across the treated cell lines, while the increased expression of CD10 was prominent in the cisplatin-resistant cell line. Isolation mediated by FACS revealed that the CD10-positive subpopulation was more refractory to cisplatin, fluorouracil and radiation than the CD10-negative subpopulation. It also showed an increased ability to form spheres in vitro and tumours in vivo. Moreover, the CD10-positive subpopulation expressed the CSC marker OCT3/4 at a higher level than that in the CD10-negative subpopulation.

Conclusions:

CD10 is associated with therapeutic resistance and CSC-like properties of HNSCC. CD10 may serve as a target molecule in the treatment of refractory HNSCC.  相似文献   
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目的探讨胰岛素样生长因子结合蛋白(insulin-like growth factor-binding protein,IGFBP)家族成员表达与非小细胞肺癌(non-small cell lung cancer,NSCLC)患者化疗效果的关系。方法收集40例NSCLC,所有患者均接受含铂药物的一线化疗方案,根据化疗疗效将患者分为化疗敏感组和不敏感组。采用酶联免疫法和免疫组化法检测两组患者血清和癌组织中的IGFBP-2、IGFBP-3和IGFBP-5的表达;分析IGFBP-3表达水平与NSCLC临床病理特征的关系;利用单因素分析和Logic多因素回归分析IGFBP-3低表达和NSCLC患者化疗不敏感的关系。结果化疗敏感组患者的血清和癌组织中IGFBP-2和IGFBP-5水平略高于化疗不敏感组,但二者差异无统计学意义(P0.05);化疗敏感组患者的血清和癌组织中的IGFBP-3显著高于化疗不敏感组,二者差异有统计学意义(P0.05)。NSCLC中发生淋巴转移和肿瘤直径较大的患者,其IGFBP-3低表达。单因素分析显示IGFBP-3低表达与化疗不敏感密切相关(OR=6.333,95%CI=1.543~26.003,P0.05)。Logistic回归多因素显示IGFBP-3低表达是患者发生化疗不敏感的独立危险因素(OR=4.093,95%CI=1.532~8.191,P0.05)。结论 IGFBP-3低表达可能引起NSCLC患者的化疗耐受,其可作为判断NSCLC患者化疗效果和预后的临床指标。  相似文献   
9.
Gallbladder cancer is the most common biliary tract malignancy and the fifth most common gastrointestinal malignancy. Chemo-resistance is the most remarkable characteristic of gallbladder cancer. The relatively dense extracellular space in tumor is the main barrier to nanotherapeutics’ anticancer efficacy. Hyaluronan (HA) was shown in our previous study to significantly improve the myxoma virus distribution via promoting the MMP-9 production, which degrades collagen IV. We demonstrated that HA increased the chemo-sensitivity of gallbladder cancer cells both in vitro and in vivo. The in vivo chemo-sensitization effect of HA could partially be due to the penetration-promoting effect of HA via degrading collagen IV.  相似文献   
10.
The transition from an epithelial to a mesenchymal phenotype (EMT) confers increased invasiveness and clonogenic potential to tumor cells. We used a breast epithelium-derived cell culture model to evaluate the impact of EMT on the cellular sensitivity towards chemotherapeutics and apoptotic stimuli. Cells that had passed through an EMT acquired resistance towards chemotherapeutics and death ligands. Mechanistically, we found that the levels of the apoptosis inhibitor Bcl-xL were strongly enhanced in mesenchymal versus epithelial cells, whereas the pro-apoptotic proteins Bim and Puma were diminished. Clinical samples from breast cancer showed enhanced Bcl-xL staining in cells that had dispersed into the desmoplastic stroma, as compared to cells that were part of large tumor cell aggregates, suggesting increased Bcl-xL expression when cells invade the stroma. Bcl-xL was necessary for apoptotic resistance in mesenchymal cells, and its expression was sufficient to confer such resistance to epithelial cells. To antagonize Bcl-xL, BH3-mimetics were used. They successfully interfered with the proliferation and survival of mesenchymal cells, and also inhibited the growth of xenograft tumors raised from the mesenchymal subpopulation. We conclude that enhanced Bcl-xL levels confer resistance to cells upon EMT, and that Bcl-xL represents a promising target for therapy directed against invasive cancer cells.  相似文献   
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