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排序方式: 共有1002条查询结果,搜索用时 15 毫秒
1.
[Objectives]To explore the inhibitory effect of AURKB gene in apoptosis and cancer cell growth in HCT 116 cells.[Methods]The in vitro cytology studies were carr... 相似文献
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AIM: To study the effect and mechanism of chlorophyllin (CHL) inhibiting HT29 cells. METHODS: IC50 value and growth curve of HT29 cells were detected with MTT method. Apoptosis was detected with Wright-Giemsa staining, FCM and DNA electrophoresis. Telomerase was detected by PCR-ELISA, and protein and mRNA expression of COX-2 gene were detected through RT-PCR and Western blot. RESULTS: CHL inhibited the growth of HT29 in a dose-dependent manner. CHL blocked HT29 cells in G1 phase but did not induce apoptosis. Different concentration of CHL inhibits the expression of telomerase and COX-2 in HT29 cells. CONCLUSION: CHL inhibited the growth of HT29 cells by inhibiting the expression of telomerase and COX-2 and blocking cells in G1 phase. 相似文献
3.
FGF4已经被证明是癌基因,它涉及肿瘤的生长和转移,为了解FGF4的表达与肿瘤微环境的关系。我们利用FGF4抗体通过免疫组化对一名肺癌患者癌旁,癌组织,癌组织小鼠移植瘤,二次移植瘤以及原代培养的细胞爬片进行FGF4检测,探究其表达差异。通过对比癌组织与对照组(癌旁组织),FGF4在癌巢中高表达;同样,移植瘤与二次移植瘤的癌巢中与癌旁组织比较,FGF4表达相对较高;但是将癌组织进行原代培养后,免疫组化检测细胞爬片FGF4,发现仅有5%±0.21%的肿瘤细胞表达FGF4,对照蛋白Cytokine作为肿瘤标记物,则在100%的肿瘤细胞中表达。研究提示免疫组化检测到FGF4在体内和体外表达不同,提示肿瘤细胞FGF4的表达与肿瘤微环境调控密切相关,肿瘤微环境对肿瘤细胞的FGF4的调控有着重要作用。 相似文献
4.
WU Xue-lei CAI Yao-wu ZHUANG Zhi-zhong CHEN Yuan-jing GUO Ren-jie ZHENG Mao-song 《园艺学报》2015,31(12):2169-2175
AIM: To explore the mechanism by which over-expression of enhancer of zeste homolog 2 (EZH2) in a panel of gastric cancer cell lines is involved in tumorigenesis of gastric cancer. METHODS: Real-time PCR and Western blot were employed to examine the mRNA and protein levels of EZH2, respectively. MTS assay, cell migration and soft agar assay were performed to investigate the role of EZH2 in the regulation of stomach cancer behaviors. The effect of EZH2 on NF-κB target gene expression was determined by Luciferase reporter and real-time PCR. Co-immunoprecipitation was used to analyze the interaction of EZH2 and p65 in HEK293T cells. RESULTS: The expression levels of EZH2 were significantly increased in the gastric cancer cells compared with normal gastric epithelial cells. Pharmacological inhibition by DZNep or knockdown of EZH2 significantly compromised AGS and SNU-16 cell activity, cell migration and anchorage-independent cell growth. Moreover, siRNA knockdown of EZH2 impaired NF-κB downstream targets, such as IL-8, CXCL5 and CCL20. In addition, the interaction of EZH2 and p65 was detected. CONCLUSION: EZH2 mediates the growth of gastric cancer cells through the regulation of NF-κB downstream gene expression. 相似文献
5.
Farzaneh Atashrazm Ray M. Lowenthal Gregory M. Woods Adele F. Holloway Joanne L. Dickinson 《Marine drugs》2015,13(4):2327-2346
There is a wide variety of cancer types yet, all share some common cellular and molecular behaviors. Most of the chemotherapeutic agents used in cancer treatment are designed to target common deregulated mechanisms within cancer cells. Many healthy tissues are also affected by the cytotoxic effects of these chemical agents. Fucoidan, a natural component of brown seaweed, has anti-cancer activity against various cancer types by targeting key apoptotic molecules. It also has beneficial effects as it can protect against toxicity associated with chemotherapeutic agents and radiation. Thus the synergistic effect of fucoidan with current anti-cancer agents is of considerable interest. This review discusses the mechanisms by which fucoidan retards tumor development, eradicates tumor cells and synergizes with anti-cancer chemotherapeutic agents. Challenges to the development of fucoidan as an anti-cancer agent will also be discussed. 相似文献
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7.
Sachiko HYOKAI Hiroyo TANAKA Noriyuki AIHARA Junichi KAMIIE 《The Journal of veterinary medical science / the Japanese Society of Veterinary Science》2021,83(3):473
In canine lymphoma, drug resistance is the major factor hindering treatment. In this study, we performed immunohistochemical examination of P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP), which are considered as transporters related to multidrug resistance in three recurrent canine lymphomas. All cases were negative for both transporters before anticancer drug administration, but became positive after this administration. The expression was confirmed in capillary endothelial cells, such as in brain capillaries acting as the blood-brain barrier (BBB). It is suggested that both transporters expressed on capillary endothelial cells in lymphoma tissue may inhibit the spread of anticancer drugs into tumor tissues from blood, the same as the BBB. Therefore, capillary endothelial cells could act as a blood-tumor barrier, which might be involved in drug resistance in canine lymphoma. 相似文献
8.
Surgical treatment of mammary carcinomas in dogs with or without postoperative chemotherapy
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This retrospective study identified prognostic factors associated with survival; and compared survival data in 94 canine mammary carcinoma (MCA) dogs treated with surgery (n = 58), or surgery and adjunct chemotherapy (n = 36), and a subset of dogs with poor prognostic factors. On multivariate analysis independent predictors of median survival time (MST) were clinical stage, lymphatic invasion (LI; present 179 days; none 1098 days), ulceration (present 118 days; none 443 days) and surgical margins (incomplete 70 days; complete 872 days). Complete surgical margins were associated with MST in dogs with stages 1–3 MCA (incomplete 68 days; complete 1098 days) and dogs with LI (incomplete 70 days; complete 347 days). There was no statistically significant improvement in MST in dogs with advanced disease (stage 4 or LI) treated with adjunctive chemotherapy (chemotherapy 228 days; none 194 days); although five dogs with complete surgical margins that received mitoxantrone and carboplatin had a mean survival of 1139 days. 相似文献
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10.
Recent studies have shown that tumour cells express tumour necrosis factor-inducible gene 6 (TSG-6) and its protein, which is known to play a key role in regulating excessive immune responses and proliferation and growth of mesenchymal stem cells (MSCs). It has not been confirmed whether the inhibition of TSG-6 for tumour cells can suppress tumour cell growth and regulate the activation of immune cells in the tumour microenvironment (TME). TSG-6-specific small interfering RNA was transfected into canine and human breast cancer cells (CIPp, CIPm and BT-20). TSG-6-down-regulated (siTSG-6) cells showed decreased cell proliferation, migration, and invasion abilities. Decreased mRNA expressions of NF-κB, STAT3 and Sox2, confirming that TSG-6 is an upper factor governing tumour growth and metastasis. Notably, siTSG-6 cells showed significantly decreased expression levels of CD44 and PD-L1. Direct and indirect co-culture of canine peripheral blood mononuclear cells (cPBMCs) and the siTSG-6 cells showed significant activation in M1 type macrophages and cytotoxic T cells. They also showed a tendency to decrease in the expression of CTLA-4 and increase in the expression of PD-1. In conclusion, this study suggests that the down-regulation of TSG-6 in breast cancer cells could not only suppress tumour growth and metastasis, and but also regulate TME. Since modulation of immune checkpoint proteins occurs in both tumour cells and immune cells, inhibiting TSG-6 and its protein within the TME could be novel therapeutic target for anticancer treatment. 相似文献