MOLECULES
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2017
·Vol. 22
·期 11
·1814
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IF 2.861
Wenrui Wang,Lingyu Zhang,Tiantian Chen,Wen Guo,Xunxia Bao,Dandan Wang,Baihui Ren,Haifeng Wang,Yu Li,Yueyue Wang,Sulian Chen,Baoding Tang,Qingling Yang,Changjie Chen
In this study, resveratrol-loaded solid lipid nanoparticles (Res-SLNs) were successfully designed to treat MDA-MB-231 cells. The Res-SLNs were prepared using emulsification and low-temperature solidification method. The Res-SLNs were spherical, with small size, negative charge, and narrow size distribution. Compared with free resveratrol, the Res-SLNs displayed a superior ability in inhibiting the proliferation of MDA-MB-231 cells. In addition, Res-SLNs exhibited much stronger inhibitory effects on the invasion and migration of MDA-MB-231 cells. Western blot analysis revealed that Res-SLNs could promote the ratio of Bax/Bcl-2 but decreased the expression of cyclinD1 and c-Myc. These results indicate that the Res-SLN may have great potential for breast cancer treatment.Keywords:solid lipid nanoparticle;resveratrol;breast cancer;cyclinD1
研究领域:
药理学
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肿瘤学
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纳米技术
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产品关联
DOI
PubMed
高影响因子
PHYTOTHERAPY RESEARCH
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2019
·Vol. 34
·期 4
·817-824
·
IF 3.766
Mingming Zhu,Xi Yu,Zongmei Zheng,Jiaming Huang,Xuepan Yang,Hongfei Shi
Cancer stem cells (CSCs) are considered as the origin and driving cells of cancer, and play a key role in the progress of cancer. Studies have shown that capsaicin exerted inhibitory effect on prostate cancer cells, however, the effects of capsaicin on prostate CSCs remain undefined. In the present study, we showed that capsaicin could downregulate prostate CSCs markers and inhibit the growth of PC-3 and DU145 prostate cancer stem cells. Further, we found capsaicin suppressed the expression of Wnt-2, p-GSK3β and β-catenin, along with downregulation of Wnt/β-catenin pathway target genes c-myc and cyclinD1. Using LiCl, a activator of Wnt/β-catenin pathway, we found activation of Wnt/β-catenin pathway could ameliorate the downregulation of prostate CSCs markers and the growth inhibition induced by capsaicin in prostate cancer stem cells. Those data suggested that the inhibition effect of capsaicin on prostate cancer stem cells and the anti-cancer effect of capsaicin on prostate cancer stem cell may be mediated by Wnt/β-catenin pathway. Findings from this study reveals for the first time the potential role and mechanisms of capsaicin on prostate cancer stem cells.
研究领域:
肿瘤学
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分子生物学
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药理学
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产品关联
DOI
PubMed
高影响因子
Inorganic Chemistry Frontiers
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2019
·Vol. 6
·期 4
·1040-1049
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IF 5.934
Yi-Gang Wu,Dong-Bo Wang,Juan-Juan Hu,Xue-Qing Song,Cheng-Zhi Xie,Zhong-Ying Ma,Jing-Yuan Xu
The design, synthesis, crystal structures and in vitro biological assessment of three iron(III) complexes, namely [Fe(L1)2]Cl (1), [Fe(L2)2]·FeCl4 (2) and [Fe(L3)(HL3)2]·(FeCl4)2·(CH3OH) (3) (HL1 = N’-(4-oxothiazolidin-2-ylidene)picolinohydrazonamide, HL2 = 2-(2-(1-(pyridin-2-yl)ethylidene)hydrazono)thiazolidin-4-one, HL3 = 3-ethyl-2-(2-(1-(pyridin-2-yl)ethylidene)hydrazono)thiazolidin-4-one, are reported in this article. Single crystal X-ray diffraction revealed that all three complexes were mononuclear molecules, approaching a coordination polyhedron of octahedral geometry, in which the 4-thiazolidinone derivative ligands exhibited different coordination modes and conformations. Their interactions with DNA were investigated by UV–visible and fluorescence spectrometries, and by agarose gel electrophoresis. Results indicated that they presented efficient DNA binding propensities and cleavage activities. In vitro, the iron(III) complexes caused cell cycle arrest at the G1 phase in response to DNA damage, effectively inhibited the cyclinD1 expression and decreased the migration of HeLa cells with a lower wound-healing rate than that of the control. Complex 3 was the most sensitive to HeLa cancer cells, followed by 2 and 1. Attractively, the tested complexes demonstrated significantly enhanced selectivity index values determined for HeLa vs. LO2 normal cells compared with cisplatin, especially for complex 3, which was up to 13.94-fold. Unlike cisplatin, more complex 3 would accumulate in HeLa cancer cells compared with LO2 normal cells.
研究领域:
无机化学
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药物化学
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肿瘤学
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分子生物学
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生物化学
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产品关联
DOI
高影响因子
Translational Cancer Research
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2019
·
IF 1.07
Heqi Bu,Dianlei Liu,Junhui Cui,Ke Cai,Feng Shen
Background Oridonin has been demonstrated to have anticancer effect on all kinds of cancer cells and it has shown anti-tumor activity in some tumors partially via the inactivation of Wnt/β-catenin signaling pathway. The study investigated the anticancer effect of oridonin on colon carcinoma cell line COLO205 and explored underlying mechanism. Methods Cell Counting Kit-8 (CCK-8) assay was performed to assess cell viability. Flow cytometry was performed to analyze the apoptosis. The key target genes and proteins involved in Wnt/β-catenin pathway were detected by quantitative polymerase chain reaction (qPCR) and Western blotting. The xenograft tumor model of colon cancer COLO205 cell was introduced to detect anti-tumor effects in vivo . Transferase-mediated dUTP nick end labeling (TUNEL) assay was adopted to test the apoptotic cells in the tumor tissues. Results Oridonin inhibited the proliferation of colon cancer COLO205 cells in a dose-dependent and time-dependent manner. Oridonin induced apoptosis by increasing the cleavage of caspases in vitro . Furthermore, the expression levels of β-catenin and its downstream targets, including c-myc, cyclinD1 and survivin were significantly reduced. Nevertheless the knockdown of β-catenin by specific small interfering RNA (siRNA) could augment the anti-proliferative and pro-apoptotic effects by oridonin in COLO205 cells. Meanwhile, oridonin also increased protein expression level of glycogen synthase kinase 3β (GSK3β) and decreased the phosphorylation level of GSK3β. In vivo , oridonin treatment significantly suppressed tumor growth of COLO205 cell xenografts, and which was accompanied by the restrain of Wnt/β-catenin pathway. Conclusions Our present study demonstrated that the growth inhibition and apoptosis induction in colon cancer COLO205 cells by oridonin could be partially mediated through discontinuing Wnt/β-catenin signaling pathway.
研究领域:
肿瘤学
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分子生物学
·
药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）