scholarly journals Biological Response to ErbB Ligands in Nontransformed Cell Lines Correlates with a Specific Pattern of Receptor Expression

Endocrinology ◽  
1998 ◽  
Vol 139 (12) ◽  
pp. 4756-4764 ◽  
Author(s):  
Srividya Sundaresan ◽  
Penelope E. Roberts ◽  
Kathleen L. King ◽  
Mark X. Sliwkowski ◽  
Jennie P. Mather
1990 ◽  
Vol 2 (10) ◽  
pp. 345-355 ◽  
Author(s):  
Lizabeth Deutsch Murphy ◽  
Eva M. Valverius ◽  
Maria Tsokos ◽  
Lyn A. Mickley ◽  
Neal Rosen ◽  
...  

Viruses ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 949
Author(s):  
Peiqi Yin ◽  
Margaret Kielian

Baby hamster kidney-21 (BHK-21) cells are widely used to propagate and study many animal viruses using infection and transfection techniques. Among various BHK-21 cell clones, the fibroblast-like BHK-21/C-13 line and the epithelial-like BHK-21/WI-2 line are commonly used cell clones for alphavirus research. Here we report that BHK-21/WI-2 cells were significantly less susceptible to primary infection by the alphavirus chikungunya virus (CHIKV) than were BHK-21/C-13 cells. The electroporation efficiency of alphavirus RNA into BHK-21/WI-2 was also lower than that of BHK-21/C-13. The growth of CHIKV was decreased in BHK-21/WI-2 compared to BHK-21/C-13, while primary infection and growth of the alphavirus Sindbis virus (SINV) were equivalent in the two cell lines. Our results suggested that CHIKV entry could be compromised in BHK-21/WI-2. Indeed, we found that the mRNA level of the CHIKV receptor MXRA8 in BHK-21/WI-2 cells was much lower than that in BHK-21/C-13 cells, and exogenous expression of either human MXRA8 or hamster MXRA8 rescued CHIKV infection. Our results affirm the importance of the MXRA8 receptor for CHIKV infection, and document differences in its expression in two clonal cell lines derived from the original BHK-21 cell cultures. Our results also indicate that CHIKV propagation and entry studies in BHK-21 cells will be significantly more efficient in BHK-21/C-13 than in BHK-21/WI-2 cells.


1996 ◽  
Vol 9 (2) ◽  
pp. 193-204 ◽  
Author(s):  
Thomas P. Prindiville ◽  
Mary C. Cantrell ◽  
Takayuki Matsumoto ◽  
William R. Brown ◽  
Aftab A. Ansari ◽  
...  

BMC Cancer ◽  
2012 ◽  
Vol 12 (1) ◽  
Author(s):  
Connie L Erickson-Miller ◽  
Kodandaram Pillarisetti ◽  
Jennifer Kirchner ◽  
David J Figueroa ◽  
Lone Ottesen ◽  
...  

Endocrinology ◽  
1993 ◽  
Vol 133 (1) ◽  
pp. 248-256 ◽  
Author(s):  
R R Denton ◽  
L P Eisen ◽  
M S Elsasser ◽  
J M Harmon

2021 ◽  
Vol 22 (6) ◽  
pp. 3160
Author(s):  
Michal Kopczynski ◽  
Malgorzata Statkiewicz ◽  
Magdalena Cybulska ◽  
Urszula Kuklinska ◽  
Katarzyna Unrug-Bielawska ◽  
...  

TNF-related apoptosis-inducing ligand (TRAIL) is a type II transmembrane protein capable of selectively inducing apoptosis in cancer cells by binding to its cognate receptors. Here, we examined the anticancer efficacy of a recently developed chimeric AD-O51.4 protein, a TRAIL fused to the VEGFA-originating peptide. We tested AD-O51.4 protein activity against human colorectal cancer (CRC) models and investigated the resistance mechanism in the non-responsive CRC models. The quantitative comparison of apoptotic activity between AD-O51.4 and the native TRAIL in nine human colorectal cancer cell lines revealed dose-dependent toxicity in seven of them; the immunofluorescence-captured receptor abundance correlated with the extent of apoptosis. AD-O51.4 reduced the growth of CRC patient-derived xenografts (PDXs) with good efficacy. Cell lines that acquired AD-O51.4 resistance showed a significant decrease in surface TRAIL receptor expression and apoptosis-related proteins, including Caspase-8, HSP60, and p53. These results demonstrate the effectiveness of AD-O51.4 protein in CRC preclinical models and identify the potential mechanism underlying acquired resistance. Progression of AD-O51.4 to clinical trials is expected.


2010 ◽  
Vol 24 (6) ◽  
pp. 1287-1296 ◽  
Author(s):  
Susan Holbeck ◽  
Jianjun Chang ◽  
Anne M. Best ◽  
Angie L. Bookout ◽  
David J. Mangelsdorf ◽  
...  

Abstract We profiled the expression of the 48 human nuclear receptors (NRs) by quantitative RT-PCR in 51 human cancer cell lines of the NCI60 collection derived from nine different tissues. NR mRNA expression accurately classified melanoma, colon, and renal cancers, whereas lung, breast, prostate, central nervous system, and leukemia cell lines exhibited heterogeneous receptor expression. Importantly, receptor mRNA levels faithfully predicted the growth-inhibitory qualities of receptor ligands in nonendocrine tumors. Correlation analysis using NR expression profiles and drug response information across the cell line panel uncovered a number of new potential receptor-drug interactions, suggesting that in these cases, individual receptor levels may predict response to chemotherapeutic interventions. Similarly, by cross-comparing receptor levels within our expression dataset and relating these profiles to existing microarray gene expression data, we defined interactions among receptors and between receptors and other genes that can now be mechanistically queried. This work supports the strategy of using NR expression profiling to classify various types of cancer, define NR-drug interactions and receptor-gene networks, predict cancer-drug sensitivity, and identify druggable targets that may be pharmacologically manipulated for potential therapeutic intervention.


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