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Point Mutation of the neu Gene in Rat Neural Tumor RT4‐AC Cells: Suppression of Tumorigenicity by s‐Myc
Forced expression of the s‐myc gene suppressed the tumorigenicity of rat RT4‐AC tumor cells in nude mice, as reported previously. Polymerase chain reaction (PCR) analysis indicated that RT4‐AC cells established from a tumor of the peripheral nervous system contain an activated neu gene with a T→A tr...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Blackwell Publishing Ltd
1990
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5917997/ https://www.ncbi.nlm.nih.gov/pubmed/1702412 http://dx.doi.org/10.1111/j.1349-7006.1990.tb02516.x |
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author | Lee, Soo‐Yong Sugiyama, Akinori Sueoka, Noboru Kuchino, Yoshiyuki |
author_facet | Lee, Soo‐Yong Sugiyama, Akinori Sueoka, Noboru Kuchino, Yoshiyuki |
author_sort | Lee, Soo‐Yong |
collection | PubMed |
description | Forced expression of the s‐myc gene suppressed the tumorigenicity of rat RT4‐AC tumor cells in nude mice, as reported previously. Polymerase chain reaction (PCR) analysis indicated that RT4‐AC cells established from a tumor of the peripheral nervous system contain an activated neu gene with a T→A transversion in the transmembrane domain. Synthesis of a protein of 60 kd in RT4‐AC cells was specifically inhibited by expression of the s‐myc gene. These results strongly suggest that s‐Myc suppresses the transforming activity of rat neural cells transformed by expression of the activated neu gene, and plays an important role in regulating expression of a cellular gene contributing to cell transformation, such as the gene that encodes the p60 protein. |
format | Online Article Text |
id | pubmed-5917997 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1990 |
publisher | Blackwell Publishing Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-59179972018-05-11 Point Mutation of the neu Gene in Rat Neural Tumor RT4‐AC Cells: Suppression of Tumorigenicity by s‐Myc Lee, Soo‐Yong Sugiyama, Akinori Sueoka, Noboru Kuchino, Yoshiyuki Jpn J Cancer Res Rapid Communication Forced expression of the s‐myc gene suppressed the tumorigenicity of rat RT4‐AC tumor cells in nude mice, as reported previously. Polymerase chain reaction (PCR) analysis indicated that RT4‐AC cells established from a tumor of the peripheral nervous system contain an activated neu gene with a T→A transversion in the transmembrane domain. Synthesis of a protein of 60 kd in RT4‐AC cells was specifically inhibited by expression of the s‐myc gene. These results strongly suggest that s‐Myc suppresses the transforming activity of rat neural cells transformed by expression of the activated neu gene, and plays an important role in regulating expression of a cellular gene contributing to cell transformation, such as the gene that encodes the p60 protein. Blackwell Publishing Ltd 1990-11 /pmc/articles/PMC5917997/ /pubmed/1702412 http://dx.doi.org/10.1111/j.1349-7006.1990.tb02516.x Text en |
spellingShingle | Rapid Communication Lee, Soo‐Yong Sugiyama, Akinori Sueoka, Noboru Kuchino, Yoshiyuki Point Mutation of the neu Gene in Rat Neural Tumor RT4‐AC Cells: Suppression of Tumorigenicity by s‐Myc |
title | Point Mutation of the neu Gene in Rat Neural Tumor RT4‐AC Cells: Suppression of Tumorigenicity by s‐Myc |
title_full | Point Mutation of the neu Gene in Rat Neural Tumor RT4‐AC Cells: Suppression of Tumorigenicity by s‐Myc |
title_fullStr | Point Mutation of the neu Gene in Rat Neural Tumor RT4‐AC Cells: Suppression of Tumorigenicity by s‐Myc |
title_full_unstemmed | Point Mutation of the neu Gene in Rat Neural Tumor RT4‐AC Cells: Suppression of Tumorigenicity by s‐Myc |
title_short | Point Mutation of the neu Gene in Rat Neural Tumor RT4‐AC Cells: Suppression of Tumorigenicity by s‐Myc |
title_sort | point mutation of the neu gene in rat neural tumor rt4‐ac cells: suppression of tumorigenicity by s‐myc |
topic | Rapid Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5917997/ https://www.ncbi.nlm.nih.gov/pubmed/1702412 http://dx.doi.org/10.1111/j.1349-7006.1990.tb02516.x |
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