Discovery of high in vitro and in vivo antitumor activities of organometallic ruthenium(ii)–arene complexes with 5,7-dihalogenated-2-methyl-8-quinolinol

2019 ◽  
Vol 48 (16) ◽  
pp. 5352-5360 ◽  
Author(s):  
Ting Meng ◽  
Qi-Pin Qin ◽  
Zi-Lu Chen ◽  
Hua-Hong Zou ◽  
Kai Wang ◽  
...  

MClClQ-RuCl induced HeLa cell apoptosis was mediated by the inhibition of telomerase activity and dysfunction of mitochondria. Remarkably, MClClQ-RuCl obviously inhibited HeLa xenograft tumor growth in vivo.

Metallomics ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 1005-1015 ◽  
Author(s):  
Qi-Pin Qin ◽  
Zhen-Feng Wang ◽  
Ming-Xiong Tan ◽  
Xiao-Ling Huang ◽  
Hua-Hong Zou ◽  
...  

MeOMBrQ-Ho induced HeLa cell apoptosis was mediated by inhibition of telomerase activity and dysfunction of mitochondria. Remarkably, MeOMBrQ-Ho obviously inhibited HeLa xenograft tumor growth in vivo.


2014 ◽  
Vol 14 (1) ◽  
pp. 67 ◽  
Author(s):  
Ingrid Labouba ◽  
Alexis Poisson ◽  
Julie Lafontaine ◽  
Nathalie Delvoye ◽  
Philippe O Gannon ◽  
...  

Tumor Biology ◽  
2013 ◽  
Vol 34 (4) ◽  
pp. 2419-2426 ◽  
Author(s):  
Baobiao Zhuo ◽  
Rong Wang ◽  
Yiyu Yin ◽  
Hongwei Zhang ◽  
Tongsheng Ma ◽  
...  

2019 ◽  
Vol 43 (21) ◽  
pp. 8146-8152 ◽  
Author(s):  
Guo-Bao Huang ◽  
Shan Chen ◽  
Qi-Pin Qin ◽  
Jin-Rong Luo ◽  
Ming-Xiong Tan ◽  
...  

3 induced NCI-H460 cell apoptosis via inhibition of the telomerase and dysfunction of mitochondria. Remarkably, 3 obviously inhibited NCI-H460 xenograft tumor growth in vivo.


2009 ◽  
Vol 57 (16) ◽  
pp. 7596-7604 ◽  
Author(s):  
Bin-Chuan Ji ◽  
Wu-Huei Hsu ◽  
Jai-Sing Yang ◽  
Te-Chun Hsia ◽  
Chi-Cheng Lu ◽  
...  

2016 ◽  
Vol 29 (4) ◽  
pp. 666-675 ◽  
Author(s):  
Pei-Hao Wen ◽  
Dong-Yu Wang ◽  
Jia-Kai Zhang ◽  
Zhi-Hui Wang ◽  
Jie Pan ◽  
...  

Kruppel-like factor 6 (KLF6) as a novel tumor suppressive gene participates in multiple biological behaviors and plays an important role in regulating tumor cell growth and invasion. However, the functions of KLF6 in hepatocellular carcinoma (HCC) remain poorly understood. The expression level of KLF6 was examined by immunohistochemical assay in human HCC tissues, and KLF6-overexpressed HCC cells (SMCC-7721 and HepG2) were used for evaluating cell proliferation and invasion by MTT and Transwell assays. A subcutaneous HCC tumor model was established for assessing tumor growth in vivo. Our results showed that the expression of KLF6 was significantly downregulated in HCC tissues compared with the adjacent non-cancerous tissues (50.0% vs. 72.0%, P = 0.034) and negatively associated with the lymph-vascular space invasion (LVSI) in HCC patients ( P = 0.003). Furthermore, overexpression of KLF6 reduced cell proliferation and weakened the cell invasive potential followed with the decreased expression of PCNA and MMP-9 in HCC cells. The in vivo experiment indicated that KLF6 overexpression suppressed the xenograft tumor growth. Therefore, our findings show that KLF6 suppresses growth and invasion of HCC cells in vitro and in vivo, suggesting a tumor suppressive function in HCC and provides the potential therapeutic target for the treatment of HCC.


PLoS ONE ◽  
2012 ◽  
Vol 7 (10) ◽  
pp. e47927 ◽  
Author(s):  
Henrike Caysa ◽  
Stefan Hoffmann ◽  
Jana Luetzkendorf ◽  
Lutz Peter Mueller ◽  
Susanne Unverzagt ◽  
...  

BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Chao Sun ◽  
Xingliang Dai ◽  
Dongliang Zhao ◽  
Haiyang Wang ◽  
Xiaoci Rong ◽  
...  

Abstract Background and objective Tumor angiogenesis is vital for tumor growth. Recent evidence indicated that bone marrow-derived mesenchymal stem cells (BMSCs) can migrate to tumor sites and exert critical effects on tumor growth through direct and/or indirect interactions with tumor cells. However, the effect of BMSCs on tumor neovascularization has not been fully elucidated. This study aimed to investigate whether fusion cells from glioma stem cells and BMSCs participated in angiogenesis. Methods SU3-RFP cells were injected into the right caudate nucleus of NC-C57Bl/6 J-GFP nude mice, and the RFP+/GFP+ cells were isolated and named fusion cells. The angiogenic effects of SU3-RFP, BMSCs and fusion cells were compared in vivo and in vitro. Results Fusion cells showed elevated levels of CD31, CD34 and VE-Cadherin (markers of VEC) as compared to SU3-RFP and BMSCs. The MVD-CD31 in RFP+/GFP+ cell xenograft tumor was significantly greater as compared to that in SU3-RFP xenograft tumor. In addition, the expression of CD133 and stem cell markers Nanog, Oct4 and Sox2 were increased in fusion cells as compared to the parental cells. Fusion cells exhibited enhanced angiogenic effect as compared to parental glioma cells in vivo and in vitro, which may be related to their stem cell properties. Conclusion Fusion cells exhibited enhanced angiogenic effect as compared to parental glioma cells in vivo and in vitro, which may be related to their stem cell properties. Hence, cell fusion may contribute to glioma angiogenesis.


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