Post-Transcriptional Deregulation of myc Genes in Lung Cancer Cell Lines
Genes of the myc family are frequently overexpressed in lung cancer. Gene amplification can explain the deregulation of these genes in a subset of tumors and cell lines, but in most cases, the cause of the elevated myc expression remains unknown. We examined whether messenger RNA (mRNA) stabilizatio...
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Published in | American journal of respiratory cell and molecular biology Vol. 23; no. 4; pp. 560 - 565 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
United States
Am Thoracic Soc
01.10.2000
American Thoracic Society |
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Abstract | Genes of the myc family are frequently overexpressed in lung cancer. Gene amplification can explain the deregulation of these genes in a subset of tumors and cell lines, but in most cases, the cause of the elevated myc expression remains unknown. We examined whether messenger RNA (mRNA) stabilization could be contributing to myc gene overexpression in lung cancer cell lines. The decay pattern of c-myc or N-myc mRNA was analyzed in 11 such cell lines and in unimmortalized human embryonic lung cells. Eight lung cancer cell lines showed stabilization of c-myc or N-myc transcripts. To determine whether this stabilization was unique to myc genes, the decay pattern of the unstable c-fos proto-oncogene mRNA was also studied. The same cell lines that exhibited stabilization of myc mRNA showed an abnormally slow decay of the c-fos message, suggesting that there might be a correlation between the abnormal decay of c-fos and myc transcripts. In contrast, the half-life of histone 2B mRNA, which is degraded in a cell cycle-specific manner, did not appear to correlate with that of myc and fos. Our results suggest that an mRNA decay pathway responsible for the destruction of unstable proto-oncogene mRNAs may be commonly affected in lung cancers. |
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AbstractList | Genes of the myc family are frequently overexpressed in lung cancer. Gene amplification can explain the deregulation of these genes in a subset of tumors and cell lines, but in most cases, the cause of the elevated myc expression remains unknown. We examined whether messenger RNA (mRNA) stabilization could be contributing to myc gene overexpression in lung cancer cell lines. The decay pattern of c-myc or N-myc mRNA was analyzed in 11 such cell lines and in unimmortalized human embryonic lung cells. Eight lung cancer cell lines showed stabilization of c-myc or N-myc transcripts. To determine whether this stabilization was unique to myc genes, the decay pattern of the unstable c-fos proto-oncogene mRNA was also studied. The same cell lines that exhibited stabilization of myc mRNA showed an abnormally slow decay of the c-fos message, suggesting that there might be a correlation between the abnormal decay of c-fos and myc transcripts. In contrast, the half-life of histone 2B mRNA, which is degraded in a cell cycle-specific manner, did not appear to correlate with that of myc and fos. Our results suggest that an mRNA decay pathway responsible for the destruction of unstable proto-oncogene mRNAs may be commonly affected in lung cancers. |
Author | Bernasconi, Nadia L Laird-Offringa, Ite A Wormhoudt, Theodora A. M |
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References | B20 B21 B22 B23 B24 B25 B26 B27 B28 B29 Hay R. J. (B19) 1996; 9 B31 B10 B32 B11 B33 Takahashi T. (B35) 1989; 49 B12 Sekido Y. (B30) 1994; 54 B34 B13 B14 B15 B17 B18 B1 B2 B4 B5 B6 B7 B8 Amy C. M. (B9) 1987; 47 |
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SubjectTerms | Blotting, Northern Gene Expression Regulation, Neoplastic Genes, myc Half-Life Humans Lung cancer Lung Neoplasms - genetics RNA Processing, Post-Transcriptional RNA, Messenger - genetics Tumor Cells, Cultured |
Title | Post-Transcriptional Deregulation of myc Genes in Lung Cancer Cell Lines |
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