In vivo selection of human renal cell carcinoma cells with high metastatic potential in nude mice

1989 ◽  
Vol 7 (4) ◽  
pp. 381-389 ◽  
Author(s):  
Seiji Naito ◽  
Shirley M. Walker ◽  
Isaiah J. Fidler
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Nude Mice ◽  
Renal Cell ◽  
Metastatic Potential ◽  
Carcinoma Cells ◽  
Human Renal Cell Carcinoma ◽  
In Vivo Selection ◽  
Selection Of

Introducing the Clusterin Gene Into Human Renal Cell Carcinoma Cells Enhances Their Metastatic Potential

2002 ◽  
Vol 167 (5) ◽  
pp. 2203-2208 ◽  
Author(s):  
HIDEAKI MIYAKE ◽  
MARTIN E. GLEAVE ◽  
SOICHI ARAKAWA ◽  
SADAO KAMIDONO ◽  
ISAO HARA
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Metastatic Potential ◽  
Carcinoma Cells ◽  
Human Renal Cell Carcinoma

scholarly journals Effects of HMGA2 on the Epithelial-Mesenchymal Transition-Related Genes in ACHN Renal Cell Carcinoma Cells-Derived Xenografts in Nude Mice

2020 ◽  
Author(s):  
Guangyao Lv ◽  
Lingling Song ◽  
Guanyu Gong ◽  
Qian Chen ◽  
Kai Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Nude Mice ◽  
Renal Cell ◽  
Epithelial Mesenchymal Transition ◽  
Human Renal Cell Carcinoma ◽  
Mesenchymal Transition

Abstract Background: The architectural transcriptional regulator high-mobility group AT-hook 2 (HMGA2) is an oncofetal protein which has been reported to be ectopically expressed in a variety of cancers. A high expression of HMGA2 in human renal cell carcinoma (RCC) is related with tumor invasiveness and poor prognosis. In the in vitro studies, HMGA2 knockdown was found to lead to decreased cell proliferation, decreased migration and changes in gene expression related with the epithelial-mesenchymal transition. Methods: In order to understand HMGA2’s effect in vivo , HMGA2 expression was knocked-down in ACHN cells using small hairpin RNA (shRNA). The HMGA2-deficient ACHN cells were xenografted into the BALB/c nude mice. The tumor growth was monitored and the expression of EMT-related genes was analyzed. Results: HMGA2 expression was confirmed to be knocked-down in the cultured and xenografted ACHN cells. The xenograft tumor of HMGA2-deficient cells demonstrated a retarded growth pattern compared with control. The expression of E-cadherin was increased, whereas N-cadherin and Snail were decreased in the HMGA2-deficient xenograft tumors. Conclusions: The present study suggested that the epigenetic regulation of EMT-related gene expression by HMGA2 exists both in the in vitro and in vivo conditions. It is likely that through this mechanism, HMGA2 regulates the cell growth in renal cell carcinoma.

scholarly journals The Role of Interleukin-6 in the Induction of Hypercalcemia in Renal Cell Carcinoma Transplanted into Nude Mice

Endocrinology ◽  
1997 ◽  
Vol 138 (5) ◽  
pp. 1879-1885 ◽  
Author(s):  
Max G. Weissglas ◽  
Denis H. J. Schamhart ◽  
Clemens W. G. M. Löwik ◽  
Socrates E. Papapoulos ◽  
Harry M. Theuns ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Serum Calcium ◽  
Nude Mice ◽  
Renal Cell ◽  
Messenger Rna ◽  
Neutralizing Antibodies ◽  
Human Renal Cell Carcinoma

Abstract Hypercalcemia is a well known complication of renal cell carcinoma (RCC). As RCCs can produce IL-6, and IL-6 may stimulate bone resorption and cause mild hypercalcemia, we examined whether IL-6 is involved in renal cancer-associated hypercalcemia in vivo. Three human renal cell carcinoma tumor lines (RC-8, RC-9, and NC-65) growing in nude mice were studied. Tumors were implanted sc, and parameters of bone metabolism and serum human IL-6 levels were determined in relation to tumor volume (TV). All three tumor lines secreted human IL-6, although in different quantities. The maximum level of IL-6 in RC-8 was 434 pg/ml (TV, 200 mm3), that in RC-9 was 81 pg/ml (TV, 1800 mm3), and that in NC-65 was 2368 pg/ml (TV, 1800 mm3). Hypercalcemia developed in RC-8 and RC-9 tumor-bearing animals, but not in NC-65-bearing animals. The hypercalcemia in both RC-8 and RC-9 tumor lines was associated with elevated levels of PTH-related peptide (PTHrP) and loss of trabecular bone volume. Serum calcium and phosphate concentrations showed an almost linear relationship with plasma PTHrP independently of the tumor line and serum IL-6 levels. No hypercalcemia occurred in the NC-65 animals, which had the highest levels of IL-6, but no detectable plasma PTHrP and PTHrP messenger RNA expression in the tumor. Administration of neutralizing antibodies to IL-6 to RC-8 animals normalized serum calcium concentrations and PTHrP values and induced a significant inhibition of tumor growth. No such effect on tumor growth of anti-IL-6 was seen in the other two tumor lines. The normalization of serum calcium in RC-8 mice is most likely attributed to the growth-inhibiting effect of anti-IL-6 on RC-8 tumor. We conclude that IL-6 secreted by RCC does not contribute directly to hypercalcemia, but may enhance hypercalcemia by stimulating the tumor growth of a subpopulation of PTHrP-secreting carcinomas.

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