Elucidating the Molecular Biomarkers Associated with Increase Responsiveness to a Cyclic Peptide CXCR4 Antagonist, LY2510924, in an Orthotopic Xenograft Mice Model on Colorectal Cancer Tumor Growth and Metastasis

2019 ◽  
Vol 229 (4) ◽  
pp. S60
Author(s):  
Raza Ahmad ◽  
David A. Margolin
Keyword(s):  
Colorectal Cancer ◽  
Tumor Growth ◽  
Cyclic Peptide ◽  
Mice Model ◽  
Cxcr4 Antagonist ◽  
Orthotopic Xenograft ◽  
Xenograft Mice Model ◽  
Cancer Tumor ◽  
Xenograft Mice ◽  
Tumor Growth And Metastasis

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 ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Mice Model ◽  
Cucurbitacin B ◽  
Xenograft Mice Model ◽  
Xenograft Mice

scholarly journals Establishment of an Orthotopic Xenograft Mice Model of Retinoblastoma Suitable for Preclinical Testing

2015 ◽  
Vol 1 (3) ◽  
pp. 200-206 ◽  
Author(s):  
Nathalie Cassoux ◽  
Aur�lie Thuleau ◽  
Franck Assayag ◽  
Isabelle Aerts ◽  
Didier Decaudin
Keyword(s):  
Mice Model ◽  
Preclinical Testing ◽  
Orthotopic Xenograft ◽  
Xenograft Mice Model ◽  
Xenograft Mice

scholarly journals Targeting Myc and Hdac8 with a Combination of SiRNAs Inhibits Tumor Growth in a Murine Neuroblastoma Xenograft Model

2020 ◽  
Vol 6 (1) ◽  
pp. 301-307
Author(s):  
Prashad N
Keyword(s):  
Nervous System ◽  
Tumor Growth ◽  
Neuroblastoma Cells ◽  
Xenograft Model ◽  
Mice Model ◽  
Xenograft Mice Model ◽  
Mycn Expression ◽  
Xenograft Mice ◽  
Combination Of Sirnas

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.

scholarly journals Polyphenolic Fraction Obtained From Thalassia testudinum Marine Plant and Thalassiolin B Exert Cytotoxic Effects in Colorectal Cancer Cells and Arrest Tumor Progression in a Xenograft Mouse Model

2020 ◽  
Vol 11 ◽  
Author(s):  
Livan Delgado-Roche ◽  
Kethia González ◽  
Fernando Mesta ◽  
Beatriz Couder ◽  
Zaira Tavarez ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Antitumor Activity ◽  
Thalassia Testudinum ◽  
Ros Generation ◽  
Mice Model ◽  
Marine Plant ◽  
Colorectal Cancer Cells ◽  
Xenograft Mice Model ◽  
Xenograft Mice

Marine plants are important sources of pharmacologically active metabolites. The aim of the present work was to evaluate the cytotoxic and antitumor activity of a polyphenolic fraction obtained from Thalassia testudinum marine plant and thalassiolin B in human colorectal cancer cells. Human cancer cell lines, including HCT15, HCT116, SW260, and HT29 were treated with tested products for cytotoxicity evaluation by crystal violet assay. The potential proapoptotic effect of these natural products was assessed by flow cytometry in HCT15 cells at 48 h using Annexin V-FITC/propidium iodide. In addition, reactive oxygen species (ROS) generation was measured by fluorescence using DCFH-DA staining, and sulfhydryl concentration by spectrophotometry. The in vivo antitumor activity of the polyphenolic fraction (25 mg/kg) was evaluated in a xenograft model in nu/nu mice. In vivo proapoptotic effect was also evaluated by immunohistochemistry using anti-caspase 3 and anti-Bcl-2 antibodies. The results showed that tested products exert colorectal cancer cell cytotoxicity. Besides, the tested products induced a significant increase (p < 0.05) of intracellular ROS generation, and a depletion of sulfhydryl concentration in HCT15 cells. The polyphenolic fraction arrested tumor growth and induced apoptosis in the xenograft mice model. These results demonstrate the cytotoxic activity of T. testudinum metabolites associated, at least, with ROS overproduction and pro-apoptotic effects. Here we demonstrated for the first time the antitumor activity of a T. testudinum polar extract in a xenograft mice model. These results suggest the potential use of T. testudinum marine plant metabolites as adjuvant treatment in cancer therapy.

scholarly journals Pectolinarigenin Suppresses the Tumor Growth in Nasopharyngeal Carcinoma

2016 ◽  
Vol 39 (5) ◽  
pp. 1795-1803 ◽  
Author(s):  
Chengyu Wang ◽  
Yin Cheng ◽  
Hongyi Liu ◽  
Yaping Xu ◽  
Hu Peng ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Tumor Growth ◽  
Cell Apoptosis ◽  
Severe Toxicity ◽  
Dependent Manner ◽  
Mice Model ◽  
Xenograft Mice Model ◽  
Subcutaneous Xenograft ◽  
Xenograft Mice

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.

scholarly journals Circular RNA hsa_circ_0043280 inhibits cervical cancer tumor growth and metastasis via miR-203a-3p/PAQR3 axis

2021 ◽  
Vol 12 (10) ◽  
Author(s):  
Chunyu Zhang ◽  
Pan Liu ◽  
Jiaming Huang ◽  
Yuandong Liao ◽  
Chaoyun Pan ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Tumor Growth ◽  
Poor Prognosis ◽  
Prognostic Biomarker ◽  
Circular Rna ◽  
Circular Rnas ◽  
Inhibit Tumor Growth ◽  
Cancer Tumor ◽  
Tumor Growth And Metastasis

AbstractCircular RNAs (circRNAs) are known to act as key regulators in a variety of malignancies. However, the role of circRNAs in cervical cancer (CCa) remains largely unknown. Herein, we demonstrated that a circRNA derived from the TADA2A gene (hsa_circ_0043280) was significantly downregulated in CCa and that this reduction in expression was correlated with a poor prognosis. Furthermore, our results demonstrated that hsa_circ_0043280 functions as a tumor suppressor to inhibit tumor growth and metastasis in CCa. Mechanistically, hsa_circ_0043280 competitively sponges miR-203a-3p and prevents miR-203a-3p from reducing the levels of PAQR3. Collectively, our results demonstrate that hsa_circ_0043280 plays a pivotal role in the development and metastasis of CCa, thus suggesting that hsa_circ_0043280 has significant potential as a prognostic biomarker and a therapeutic target for CCa.

scholarly journals Co-Treatment with the Epigenetic Drug, 3-Deazaneplanocin A (DZNep) and Cisplatin after DZNep Priming Enhances the Response to Platinum-Based Therapy in Chondrosarcomas

Cancers ◽  
2021 ◽  
Vol 13 (18) ◽  
pp. 4648
Author(s):  
Eva Lhuissier ◽  
Juliette Aury-Landas ◽  
Marion Lenté ◽  
Karim Boumediene ◽  
Catherine Baugé
Keyword(s):  
Tumor Volume ◽  
Mice Model ◽  
Antitumoral Effect ◽  
Viable Cells ◽  
Epigenetic Drug ◽  
Xenograft Mice Model ◽  
Xenograft Mice ◽  
Tumoral Cells

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.

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