Design and Synthesis of a Fluoroindolocarbazole Series as Selective Topoisomerase I Active Agents. Discovery of Water-Soluble 3,9-Difluoro-12,13-dihydro-13-[6-amino-β-d-glucopyranosyl]-5H,13H-benzo[b]- thienyl[2,3-a]pyrrolo[3,4-c]carbazole- 5,7(6H)-dione (BMS-251873) with Curative Antitumor Activity against Prostate Carcinoma Xenograft Tumor Model§

2004 ◽  
Vol 47 (7) ◽  
pp. 1609-1612 ◽  
Author(s):  
Balu N. Balasubramanian ◽  
Denis R. St. Laurent ◽  
Mark G. Saulnier ◽  
Byron H. Long ◽  
Carol Bachand ◽  
...  
Keyword(s):  
Antitumor Activity ◽  
Prostate Carcinoma ◽  
Topoisomerase I ◽  
Tumor Model ◽  
Water Soluble ◽  
Xenograft Tumor ◽  
Design And Synthesis ◽  
Xenograft Tumor Model ◽  
Carcinoma Xenograft

scholarly journals Ocotillol Enhanced the Antitumor Activity of Doxorubicin via p53-Dependent Apoptosis

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Hongbo Wang ◽  
Pengfei Yu ◽  
Jing Bai ◽  
Jianqiao Zhang ◽  
Liang Kong ◽  
...  
Keyword(s):  
Antitumor Activity ◽  
Cell Apoptosis ◽  
Therapeutic Strategy ◽  
Target Genes ◽  
Tumor Model ◽  
Xenograft Tumor ◽  
Xenograft Tumor Model ◽  
Hoechst Staining ◽  
Dose Dependent ◽  
Mtt Assays

The use of doxorubicin (Dox) was severely constrained by dose-dependent side effects, which might be attenuated by combining a “sensitizer” to decrease its cumulative dosage. In this study, it was investigated whether ocotillol could enhance the antiproliferation activity of Dox. MTT assays and xenograft tumor model were firstly conducted to evaluate the effect of ocotillol on the antitumor activity of Dox. Flow cytometry and Hoechst staining assays were then performed to assess cell apoptosis. Western blot and real-time PCR were finally used to detect the expression of p53 and its target genes. Our results showed ocotillol to enhance Dox-induced cell death in p53 wild-type cancer cells. Compared with Dox alone, Dox with ocotillol (Dox-O) could induce much more cell apoptosis and activate p53 to a much greater degree, which in turn markedly increased expression of proapoptosis genes. The enhanced cytotoxic activity was partially blocked by pifithrin-α, which might be through attenuating the increased apoptosis. Furthermore, ocotillol significantly increased the antitumor activity of Dox in A549 xenograft tumor in nude mice. These findings indicated that ocotillol could potentiate the cytotoxic effect of Dox through p53-dependent apoptosis and suggested that coadministration of ocotillol with Dox might be a potential therapeutic strategy.

Responsiveness of Human Prostate Carcinoma Bone Tumors to Interleukin-2 Therapy in a Mouse Xenograft Tumor Model

1999 ◽  
Vol 23 (5) ◽  
pp. 408-416 ◽  
Author(s):  
Sosa V. Kocheril ◽  
David J. Grignon ◽  
Ching Y. Wang ◽  
Richard L. Maughan ◽  
Emily J. Montecillo ◽  
...  
Keyword(s):  
Prostate Carcinoma ◽  
Bone Tumors ◽  
Interleukin 2 ◽  
Tumor Model ◽  
Human Prostate ◽  
Xenograft Tumor ◽  
Mouse Xenograft ◽  
Human Prostate Carcinoma ◽  
Xenograft Tumor Model

Antitumor Activity of γδ T Cells Reactive against Cytomegalovirus-Infected Cells in a Mouse Xenograft Tumor Model

2009 ◽  
Vol 69 (9) ◽  
pp. 3971-3978 ◽  
Author(s):  
Christel Devaud ◽  
Eric Bilhere ◽  
Séverine Loizon ◽  
Vincent Pitard ◽  
Charlotte Behr ◽  
...  
Keyword(s):  
T Cells ◽  
Antitumor Activity ◽  
Γδ T Cells ◽  
Tumor Model ◽  
Xenograft Tumor ◽  
Mouse Xenograft ◽  
Xenograft Tumor Model ◽  
Infected Cells

scholarly journals Wnt5b-induced PCP/JNK Activation Promotes PD-L1 Expression and the Malignant Phenotype of Non-small Cell Lung Cancer 

2020 ◽  
Author(s):  
Guangping Wu ◽  
Yuan Luo ◽  
Yusai Xie ◽  
Yang Han ◽  
Di Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Tumor Model ◽  
Small Cell ◽  
Xenograft Tumor ◽  
Small Cell Lung ◽  
Malignant Phenotype ◽  
Membrane Recruitment ◽  
Xenograft Tumor Model

Abstract Background: Wnt5b is noncanonical Wnt ligand, and programmed-death ligand 1 (PD-L1) is a targeted agent for immunotherapy, but the mechanism by which Wnt5b regulates PD-L1 expression in non-small cell lung cancer (NSCLC) is unclear. Methods: Wnt5b and PD-L1 expressions were detected in NSCLC specimens by immunohistochemistry. The interrelationship connecting Wnt5b with PD-L1 was verified using dual-luciferase assay, immunofluorescence, coimmunoprecipitation, western blot，real-time PCR and xenograft tumor model. Results: Wnt5b and PD-L1 expressions were positively correlated in NSCLC specimens. Five-year survival time in the group with their coexpression was significantly lower than that without coexpression. Under the effect of Wnt5b, Frizzled-3 (Fzd3) initiated Dishevellde-3 (Dvl-3) membrane recruitment via DEP domain by Dvl-3 phosphorylation, contributing to activate PCP/JNK signaling through the small GTPase Rac1, and then upregulate PD-L1 expression and promote the malignant phenotype of NSCLC in vivo and in vitro. After PD-L1 antibody treatment, Wnt5b induced tumor growth was inhibited significantly in xenograft tumor model. Conclusion: We demonstrate a new signal transduction pathway: Wnt5b initiates Dvl-3 membrane recruitment via DEP domain by Fzd3 so as to promote Rac1–PCP/JNK–PD-L1 pathway, which provides a potential target for clinical intervention and immunotherapy in lung cancer.

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