Conversion of a Poorly Differentiated Human Adenocarcinoma to Ascites Form With Invasion and Metastasis in Nude Mice: Brief Communication

1978 ◽  
Vol 60 (4) ◽  
pp. 925-929 ◽  
Author(s):  
Seiichi Takahashi ◽  
Yoichi Konishi ◽  
Katsunori Nakatani ◽  
Shoji Inui ◽  
Kiyohide Kojima ◽  
...  
Keyword(s):  
Nude Mice ◽  
Invasion And Metastasis ◽  
Poorly Differentiated ◽  
Ascites Form

Nude mice with lacZ transduced human tumor xenografts as an in vivo model for invasion and metastasis

Lung Cancer ◽  
1991 ◽  
Vol 7 ◽  
pp. 30 ◽  
Author(s):  
Mogens Spang-Thomsen ◽  
James A. Zwiebel ◽  
Jørgen Rygaard ◽  
Nils Brünner
Keyword(s):  
Nude Mice ◽  
Human Tumor ◽  
In Vivo Model ◽  
Invasion And Metastasis ◽  
Human Tumor Xenografts ◽  
Tumor Xenografts

scholarly journals N-α-Acetyltransferase 10 protein inhibits invasion and metastasis of oral squamous cell carcinoma via regulating Pirh2-p53 signaling pathway

2020 ◽  
Author(s):  
Fazhan Wang ◽  
Jun Zheng ◽  
Yongyong Yang ◽  
Jie Yang ◽  
Ting Luo ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Squamous Cell ◽  
Nude Mice ◽  
Invasion And Metastasis ◽  
P53 Signaling ◽  
P53 Signaling Pathway

Abstract Background Naa10p (N-α-Acetyltransferase 10 protein) was reported to be involved in tumor invasion and metastasis in several of tumors. However, the role and mechanism of Naa10p mediated invasion and metastasis in oral squamous cell carcinoma (OSCC) remains undetermined. Methods The functional role of Naa10p in OSCC cells were determined using Transwell assay in vitro and xenograft tumorigenesis in nude mice. Immunoprecipitation, GST-pull down assays and immunofluorescence were performed to confirm the interaction between Naa10p and RelA/p65 in OSCC cells. Lastly, luciferase reporter assays, chromatin immunoprecipitation (ChIP) and western blot were used to evalute the effect of Naa10p expression on the Pirh2-p53 signaling pathway. Results Naa10p inhibits cell migration and invasion in vitro and attenuates the xenograft tumorigenesis in nude mice. Mechanistically, there is a physical interaction between Naa10p and RelA/p65 in OSCC cells, thereby preventing RelA/p65-mediated transcriptional activation of Pirh2. Consequently, inhibition of Pirh2 increased p53 level and suppressed the expression of p53 downstream targets, MMP-2 and MMP-9. Conclusion Naa10p function as a tumor metastasis suppressor in the progression of OSCC by targeting Pirh2-p53 axis, and might be a prognostic marker as well as a therapeutic target for OSCC.

Ascites Form of a Human Cancer Serially Transplantable in Nude Mice

1976 ◽  
Vol 57 (4) ◽  
pp. 965-967 ◽  
Author(s):  
Voshito Ueyama ◽  
Vukio Kondo ◽  
Norikazu Tamaoki ◽  
Nakaaki Ohsawa
Keyword(s):  
Nude Mice ◽  
Human Cancer ◽  
Ascites Form

Tumorigenicity, invasion, and metastasis of human gastric cancer in nude mice

1991 ◽  
Vol 117 (6) ◽  
pp. 533-538 ◽  
Author(s):  
Sonshin Takao ◽  
Hisaaki Shimazu ◽  
Shigeho Maenohara ◽  
Schuichi Hokita ◽  
Takashi Aikou
Keyword(s):  
Gastric Cancer ◽  
Nude Mice ◽  
Human Gastric Cancer ◽  
Invasion And Metastasis

scholarly journals Anti-miR182 Reduces Ovarian Cancer Burden, Invasion, and Metastasis: An In Vivo Study in Orthotopic Xenografts of Nude Mice

2014 ◽  
Vol 13 (7) ◽  
pp. 1729-1739 ◽  
Author(s):  
Xiaofei Xu ◽  
Bushra Ayub ◽  
Zhaojian Liu ◽  
Vanida Ann Serna ◽  
Wenan Qiang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Nude Mice ◽  
In Vivo Study ◽  
Invasion And Metastasis ◽  
Cancer Burden ◽  
Orthotopic Xenografts

scholarly journals CAB39 mediates epithelial-mesenchymal transition via activation of NF-κB signaling to facilitate bladder cancer invasion and metastasis

2021 ◽  
Author(s):  
Haichao Chao ◽  
Lifen Peng ◽  
Leihong Deng ◽  
Zhaojun Yu ◽  
Huanhuan Deng ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Lines ◽  
Nude Mice ◽  
Molecular Mechanisms ◽  
Epithelial Mesenchymal Transition ◽  
Biological Activities ◽  
Expression Patterns ◽  
Critical Role ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition

Abstract Background Bladder cancer (BC) is the most common urinary cancer among men with a high mortality rate despite of constant advancement in medical and therapeutic treatment. Recent evidence demonstrated that CAB39 plays a critical role in BC pathogenesis by exhibiting various biological activities, but the underlying molecular mechanisms remain unclear. The aim of this research was to define the expression patterns of CAB39 in normal and tumor tissues and explore its biological function in epithelia-mesenchymal transition (EMT) in human BC. Methods Immunohistochemistry and Quantitative RT-PCR analyses were used respectively to examine the expression of CAB39 in BC tissues and cell lines with different metastatic potentials. In addition, the clinical significance of CAB39 expression was also evaluated. Wound-healing assay, cell invasion assay, and CCK8 proliferation assay in cell lines in which CAB39 was knocked down by shRNA, as well as xenograft tumor models in nude mice, were performed to assess the effect of CAB39 reduction on invasion, migration, and proliferation of BC cells. The GSEA database was used to analyze panel of genes enriched as a result of elevated CAB39 expression in BC cells, and the results were validated by western blot analysis. Results The level of CAB39 protein was up-regulated in invasive but not in noninvasive bladder cancer tissues. Elevated expression of CAB39 was inversely correlated with prognosis of the malignant disease. Additionally, CAB39 was differentially expressed in T24, 5637, and J82 bladder cancer cell lines with highest expression in T24, the most invasive cell line among the three. However, shRNA-mediated attenuation of endogenous CAB39 in T24 and 5637 cell lines reversed such invasive and metastatic effects as demonstrated by the inhibition of tumorigenesis in nude mice xenografts. Furthermore, we demonstrated that CAB39 could mediate EMT through upregulation of N-cadherin and downregulation of E-cadherin in BC via NF-kB signaling pathway. Conclusions Our study reveals a previously unknown mechanism of CAB39-mediated EMT in promoting invasion and metastasis of BC and provides a rationale for future investigation of CAB39 as a potential target for the development of novel therapeutic agents to fight the malignancy.

scholarly journals High PHD Finger Protein 19 (PHF19) expression predicts poor prognosis in colorectal cancer: a retrospective study

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e11551
Author(s):  
Pengfei Li ◽  
Jie Sun ◽  
Yuanyuan Ruan ◽  
Lujun Song
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Western Blot ◽  
Nude Mice ◽  
Tumor Formation ◽  
Tumor Proliferation ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition ◽  
Proliferative Ability

Background Colorectal cancer (CRC) is the third most common cancer all around the world, and it seriously threats human health. PHF19 has been proved to be closely related to the prognosis of patients in a variety of malignant tumors, but the effect of PHF19 on the prognosis evaluation of CRC patients has not been confirmed. Methods In our study, we used GEO, TCGA database and IHC to verify the PHF19 expression in CRC samples. Survival analysis of PHF19 based on TCGA, GEO series, and our own CRC sample were performed. Cox regression was performed to reveal the relationship between PHF19 and prognosis. Co-expression was performed to find genes related to PHF19 expression. GO/KEGG enrichment analysis and GSEA analysis were used to confirm the most relevant signal pathway to PHF19. Next, cell experiments were performed to verify the effect of PHF19 on the proliferation, invasion and metastasis of CRC. Then, Western blot was used to verify the protein expression of the above two phenotypes. Finally, tumor formation experiments in nude mice were used to verify the role of PHF19 of tumor proliferation in vivo. Results We found that PHF19 was significantly over-expressed in tumors compared with normal tissues. Kaplan–Meier (K–M) analysis indicated that high PHF19 in CRC associated with poor overall survival (OS) in CRC patients. Clinical correlation analysis showed that high expression of PHF19 was closely related to t umor progression in CRC patients, especially infiltration and metastasis. Bioinformatics revealed that PHF19 might affect tumor malignant phenotype by regulating the cell cycle in CRC. CCK-8 and clonal formation experiment showed that the proliferative ability of tumor cells was promoted. Flow cytometry showed that the cell cycle accelerated the transition from G1 to S phase. Western blot found that Cyclin D1, CDK4, and CDK6 expression were up-regulated. Transwell and wound-healing experiment found that invasive and migratory abilities was promoted after the over-expression of PHF19. Western blot showed that the expression of key proteins of Epithelial-Mesenchymal Transition (EMT) changed. Tumor formation experiments in nude mice showed that overexpression of PHF19 could promote tumor proliferation in vivo. Conclusion Our research proved that PHF19 could be an independent prognostic factor for CRC, PHF19 promoted the proliferative ability and the invasion and metastasis of CRC by up-regulating the expression of key molecules related to cell cycle and EMT pathway in vitro, promoting tumor proliferation in vivo.

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