Role of COX-2 in Comedo-type Formations in a Mouse Xenograft Model of Canine Mammary Comedocarcinoma

2012 ◽  
Vol 146 (1) ◽  
pp. 83
Author(s):  
L. Camacho ◽  
J.C. Illera ◽  
A. González-Gil ◽  
Ma.J. Illera ◽  
Ma.D. Pérez-Alenza ◽  
...  
Keyword(s):  
Xenograft Model ◽  
Mouse Xenograft ◽  
Mouse Xenograft Model ◽  
Cox 2

scholarly journals Oncogenic lncRNA ZNF561-AS1 is essential for colorectal cancer proliferation and survival through regulation of miR-26a-3p/miR-128-5p-SRSF6 axis

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Zizhen Si ◽  
Lei Yu ◽  
Haoyu Jing ◽  
Lun Wu ◽  
Xidi Wang
Keyword(s):  
Colorectal Cancer ◽  
Rna Binding ◽  
Xenograft Model ◽  
Luciferase Reporter ◽  
Cancer Proliferation ◽  
Mouse Xenograft ◽  
Mouse Xenograft Model

Abstract Background Long non-coding RNAs (lncRNA) are reported to influence colorectal cancer (CRC) progression. Currently, the functions of the lncRNA ZNF561 antisense RNA 1 (ZNF561-AS1) in CRC are unknown. Methods ZNF561-AS1 and SRSF6 expression in CRC patient samples and CRC cell lines was evaluated through TCGA database analysis, western blot along with real-time PCR. SRSF6 expression in CRC cells was also examined upon ZNF561-AS1 depletion or overexpression. Interaction between miR-26a-3p, miR-128-5p, ZNF561-AS1, and SRSF6 was examined by dual luciferase reporter assay, as well as RNA binding protein immunoprecipitation (RIP) assay. Small interfering RNA (siRNA) mediated knockdown experiments were performed to assess the role of ZNF561-AS1 and SRSF6 in the proliferative actives and apoptosis rate of CRC cells. A mouse xenograft model was employed to assess tumor growth upon ZNF561-AS1 knockdown and SRSF6 rescue. Results We find that ZNF561-AS1 and SRSF6 were upregulated in CRC patient tissues. ZNF561-AS1 expression was reduced in tissues from treated CRC patients but upregulated in CRC tissues from relapsed patients. SRSF6 expression was suppressed and enhanced by ZNF561-AS1 depletion and overexpression, respectively. Mechanistically, ZNF561-AS1 regulated SRSF6 expression by sponging miR-26a-3p and miR-128-5p. ZNF561-AS1-miR-26a-3p/miR-128-5p-SRSF6 axis was required for CRC proliferation and survival. ZNF561-AS1 knockdown suppressed CRC cell proliferation and triggered apoptosis. ZNF561-AS1 depletion suppressed the growth of tumors in a model of a nude mouse xenograft. Similar observations were made upon SRSF6 depletion. SRSF6 overexpression reversed the inhibitory activities of ZNF561-AS1 in vivo, as well as in vitro. Conclusion In summary, we find that ZNF561-AS1 promotes CRC progression via the miR-26a-3p/miR-128-5p-SRSF6 axis. This study reveals new perspectives into the role of ZNF561-AS1 in CRC.

Abstract 1347: A human-mouse xenograft model to study the role of TSLP in CRLF2d B-ALL

2012 ◽  
Author(s):  
Kimberly J. Payne ◽  
Rui-Jun Su ◽  
Olivia L. Francis ◽  
Shannalee R. Martinez ◽  
Terrence Bennett ◽  
...  
Keyword(s):  
Xenograft Model ◽  
Mouse Xenograft ◽  
Mouse Xenograft Model

Abstract B21: A human-mouse xenograft model to evaluate therapies and study the role of TSLP-induced signals in Ph-like ALL

2014 ◽  
Author(s):  
Olivia Francis ◽  
Ruijun Su ◽  
Shannalee Martinez ◽  
Ineavely Baez ◽  
Terry-Ann Milford ◽  
...  
Keyword(s):  
Xenograft Model ◽  
Mouse Xenograft ◽  
Mouse Xenograft Model

Abstract B25: A human-mouse xenograft model to evaluate therapies and study the role of TSLP-induced signals in Ph-like ALL

2014 ◽  
Author(s):  
Ruijun Su ◽  
Francis L. Olivia ◽  
Shannalee R. Martinez ◽  
Ineavely Baez ◽  
Terry Ann Milford ◽  
...  
Keyword(s):  
Xenograft Model ◽  
Mouse Xenograft ◽  
Mouse Xenograft Model

scholarly journals Inhibitory role of ATF3 in gastric cancer progression through regulating cell EMT and stemness

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Chuanqian Huang ◽  
Renli Chen ◽  
Fangjing Zheng ◽  
Yirong Tang ◽  
Xiukang Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Colony Formation ◽  
Epithelial Mesenchymal Transition ◽  
Xenograft Model ◽  
Mesenchymal Transition ◽  
Mouse Xenograft ◽  
Mouse Xenograft Model

Abstract Background Gastric cancer (GC) is one of the most common cancers and the third leading cause of cancer related mortality worldwide. The 5-year survival rate is rather low owing to advanced unresectable and distant metastasis. The EMT has been widely implicated in the stemness, metastatic dormancy, and chemoresistance of different solid tumors. Given the fact that activating transcription factor-3 (ATF3) is a member of the ATF/CREB family of transcription factors and its role in regulation of GC recurrence and metastasis remain poorly understood, the aim of the present study was to investigate its potential impact in epithelial–mesenchymal transition (EMT) and cancer stem cell (CSC) properties and GC aggression. Methods To elucidate the potential role of ATF3 in gastric cancer, we utilized SGC-7901 and MGC-803 gastric cancer cell lines as research models and constructed stable cell lines overexpressing ATF3. We conducted a series of assays including cell proliferation, colony formation, cell migration, tumorsphere formation, and invasion to investigate the functional roles of ATF3 in stemness of gastric cancer. The possible effect of ATF3 on epithelial–mesenchymal transition (EMT) was assessed through flow cytometry and qRT-PCR. In vivo functional effect of upregulation of ATF3 on tumor growth was examined in a mouse xenograft model. Results We found that overexpression of ATF3 inhibited cell proliferation, colony formation, cell migration and invasion. In addition, up-regulation of ATF3 attenuated tumorsphere formation, cell stemness, and potentially decreased expression of EMT markers. Moreover, ATF3 overexpression inhibited tumorigenesis in mouse xenograft model. Conclusion Our data suggest a suppressive role of ATF3 in gastric cancer development. Our findings will provide a potential therapeutic strategy and novel drug target for gastric cancer.

scholarly journals A Disintegrin and Metalloprotease 12 Promotes Tumor Progression by Inhibiting Apoptosis in Human Colorectal Cancer

Cancers ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1927
Author(s):  
Young-Lan Park ◽  
Sun-Young Park ◽  
Hyung-Hoon Oh ◽  
Min-Woo Chung ◽  
Ji-Yun Hong ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle Progression ◽  
Xenograft Model ◽  
Tumor Formation ◽  
Depth Of Invasion ◽  
Mouse Xenograft ◽  
Mouse Xenograft Model ◽  
Tumor Cell Behavior ◽  
Model Tumor

A disintegrin and metalloprotease 12 (ADAM12) has been implicated in cell growth, tumor formation, and metastasis. Therefore, we evaluated the role of ADAM12 in colorectal cancer (CRC) progression and prognosis, and elucidated whether targeted downregulation of ADAM12 could lead to therapeutic sensitization. The effect of ADAM12 on tumor cell behavior was assessed in CRC cell lines, CRC tissues, and a mouse xenograft model. ADAM12 overexpression enhanced proliferation, inhibited apoptosis, and acted as positive regulator of cell cycle progression in CRC cells. Phosphorylation of PTEN was decreased and that of Akt was increased by ADAM12 overexpression. These results were reversed upon ADAM12 knockdown. ADAM12 overexpression was significantly associated with the cancer stage, depth of invasion, lymph node metastasis, distant metastasis, and poor survival in CRC patients. In a mouse xenograft model, tumor area, volume, and weight were significantly greater for the ADAM12-pcDNA6-myc-transfected group than for the empty-pcDNA6-myc-transfected group, and significantly lower for the ADAM12-pGFP-C-shLenti-transfected group than for the scrambled pGFP-C-shLenti-transfected group. In conclusion, ADAM12 overexpression is essential for the growth and progression of CRC. Furthermore, ADAM12 knockdown reveals potent anti-tumor activity in a mouse xenograft model. Thus, ADAM12 may serve as a promising biomarker and/or therapeutic target in CRC.

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