scholarly journals A Bioreductive Prodrug of Cucurbitacin B Significantly Inhibits Tumor Growth in the 4T1 Xenograft Mice Model

2019 ◽  
Vol 10 (10) ◽  
pp. 1400-1406 ◽  
Author(s):  
Parichat Suebsakwong ◽  
Jie Wang ◽  
Phorntip Khetkam ◽  
Natthida Weerapreeyakul ◽  
Jing Wu ◽  
...  
2020 ◽  
Vol 6 (1) ◽  
pp. 301-307
Author(s):  
Prashad N

Neuroblastoma is a common tumor of the peripheral nervous system in children. Highly aggressive MYC-drivenneuroblastoma is defined by increased MYC and/or MYCN expression. HDAC8 overexpression is associated with advanced neuroblastoma. Previously, we have demonstrated that transient knockdown of both Myc and Hdac8 using siRNA significantly suppressed neuroblastoma cells proliferation compared to knockdown of either target in vitro. In this study, we further investigated whether combinational targeting Myc and Hdac8 in neuroblastoma xenograft mice model is consistent with our previous findings. Intratumoral treatment with siRNA-MYC and siRNA-HDAC8 reduced the levels of the target MYC protein by 64% and HDAC8 by 85%; in addition, we found that the average tumor growth was reduced by 80% compared to that of control tumors treated with NC-siRNA. Our results suggest the potential therapeutic effect of the combination of siRNA-MYC and siRNA-HDAC8 for neuroblastoma treatment.


2016 ◽  
Vol 39 (5) ◽  
pp. 1795-1803 ◽  
Author(s):  
Chengyu Wang ◽  
Yin Cheng ◽  
Hongyi Liu ◽  
Yaping Xu ◽  
Hu Peng ◽  
...  

Background/Aims: Nasopharyngeal cancer (NPC) is one of the common human malignant diseases all over the world, and chemotherapy remains the main therapy for NPC. However, the survival and life quality of NPC patients are still very poor. Thus, novel and selective anti-tumor agents are pressingly needed. Our previous study identified pectolinarigenin as a novel effective anti-tumor drug candidate for NPC. In this study, we further investigated its anti-tumor activities and explored the potential molecular mechanism. Methods: NPC C666-1 cells were cultured and treated by pectolinarigenin. Cell proliferation assay, colony formation assay, Transwell assay and wound healing assay were conducted and cell apoptosis was detected by flow cytometry. Mitochondrial transmembrane potential and ROS were also observed. NPC subcutaneous xenograft mice model was established to evaluate the anti-tumor effect of pectolinarigenin in vivo. Results: We observed that treatment of pectolinarigenin inhibited cell viability and cell migration of NPC C666-1 cells in concentration- and time-dependent manner. Pectolinarigenin induced cell apoptosis in C666-1 cells detected by flow cytometry analysis, which was associated with the activation of mitochondrial-related apoptosis and the accumulation of reactive oxygen species (ROS). Pectolinarigenin also activated caspase signaling pathway. The in vivo experiment of subcutaneous xenograft mice model also indicated that the administration of pectolinarigenin could decrease the tumor growth of NPC and no severe toxicity was observed. Conclusions: Based on our findings, we conclude that pectolinarigenin could suppress the tumor growth of NPC, which verifies it as a new therapeutic agent for treating this devastating disease.


Cancers ◽  
2021 ◽  
Vol 13 (18) ◽  
pp. 4648
Author(s):  
Eva Lhuissier ◽  
Juliette Aury-Landas ◽  
Marion Lenté ◽  
Karim Boumediene ◽  
Catherine Baugé

Background: We have previously shown that 3-Deazaneplanocin A (DZNep) induces apoptosis in chondrosarcomas. Herein, we tested whether the combination of this epigenetic drug to a standard anticancer therapy may enhance the response to each drug in these bone tumors. Methods: Two chondrosarcoma cell lines (SW1353 and JJ012) were cultured in the presence of DZNep and/or cisplatin. Cell growth was evaluated by counting viable cells, and apoptosis was determined by Apo2.7 expression by flow cytometry. In vivo, the antitumoral effect of the DZNep/cisplatin combination was assessed through measurements of tumor volume of JJ012 xenografts in nude mice. Results: In vitro, the DZNep/cisplatin combination reduced cell survival and increased apoptosis compared to each drug alone in chondrosarcomas, but not in normal cells (chondrocytes). This enhancement of the antitumoral effect of the DZNep/cisplatin combination required a priming incubation with DZNep before the co-treatment with DZNep/cisplatin. Furthermore, in the chondrosarcoma xenograft mice model, the combination of both drugs more strongly reduced tumor growth and induced more apoptosis in tumoral cells than each of the drugs alone. Conclusion: Our results show that DZNep exposure can presensitize chondrosarcoma cells to a standard anticancer drug, emphasizing the promising clinical utilities of epigenetic-chemotherapeutic drug combinations in the future treatment of chondrosarcomas.


2015 ◽  
Vol 1 (3) ◽  
pp. 200-206 ◽  
Author(s):  
Nathalie Cassoux ◽  
Aur�lie Thuleau ◽  
Franck Assayag ◽  
Isabelle Aerts ◽  
Didier Decaudin

2017 ◽  
Vol 19 (suppl_3) ◽  
pp. iii55-iii56
Author(s):  
M. Da Ros ◽  
A. Iorio ◽  
O. Fantappiè ◽  
V. De Gregorio ◽  
L. Bonaccorsi ◽  
...  

PLoS ONE ◽  
2014 ◽  
Vol 9 (2) ◽  
pp. e90349 ◽  
Author(s):  
Lu Dai ◽  
Jimena Trillo-Tinoco ◽  
Lihua Bai ◽  
Baoli Kang ◽  
Zengguang Xu ◽  
...  

Biomaterials ◽  
2010 ◽  
Vol 31 (8) ◽  
pp. 2435-2445 ◽  
Author(s):  
Rohidas B. Arote ◽  
Soon-Kyung Hwang ◽  
Hwang-Tae Lim ◽  
Tae-Hee Kim ◽  
Dhananjay Jere ◽  
...  

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