Differential expression of myc, max and RB1 genes in human gliomas and glioma cell lines
- PMID: 8286200
- PMCID: PMC1968776
- DOI: 10.1038/bjc.1994.3
Differential expression of myc, max and RB1 genes in human gliomas and glioma cell lines
Abstract
Deregulated expression of myc proto-oncogenes is implicated in several human neoplasias. We analysed the expression of c-myc, N-myc, L-myc, max and RB1 mRNAs in a panel of human gliomas and glioma cell lines and compared the findings with normal neural cells. The max and RB1 genes were included in the study because their protein products can interact with the Myc proteins, being thus putative modulators of Myc activity. Several gliomas contained c/L-myc mRNAs at levels higher than those in fetal brain, L-myc predominantly in grade II/III and c-myc in grade III gliomas. High-level N-myc expression was detected. In one small-cell glioblastoma and lower levels in five other gliomas. In contrast, glioma cell lines totally lacked N/L-myc expression. The in situ hybridisations revealed mutually exclusive topographic distribution of myc and glial fibrillary acidic protein (GFAP) mRNAs, and a lack of correlation between myc expression and proliferative activity, max and RB1 mRNAs were detected in most tumours and cell lines. The glioma cells displayed interesting alternative splicing patterns of max mRNAs encoding Max proteins which either suppress (Max) or augment (delta Max) the transforming activity of Myc. We conclude that (1) glioma cells in vivo may coexpress several myc genes, thus resembling fetal neural cells; but (2) cultured glioma cells expression only c-myc; (3) myc, max and RB1 are regulated independently in glioma cells; and (4) alternative processing of max mRNA in some glioma cells results in delta Max encoding mRNAs not seen in normal fetal brain.
Similar articles
-
Expression of oligodendrocytic mRNAs in glial tumors: changes associated with tumor grade and extent of neoplastic infiltration.Cancer Res. 1997 Sep 15;57(18):4098-104. Cancer Res. 1997. PMID: 9307299
-
Differential expression of c-myc, max and mxi1 in human myeloid leukemia cells during retrodifferentiation and cell death.Leuk Res. 1995 Oct;19(10):699-705. doi: 10.1016/0145-2126(95)00040-u. Leuk Res. 1995. PMID: 7500645
-
Expression of glial fibrillary acidic protein, vimentin, fibronectin, and N-myc oncoprotein in primary human brain tumor cell explants.Pediatr Neurosurg. 1991-1992;17(4):169-74. doi: 10.1159/000120590. Pediatr Neurosurg. 1991. PMID: 1668298
-
myc, max, and a novel rlf-L-myc fusion protein in small-cell lung cancer.Princess Takamatsu Symp. 1991;22:307-18. Princess Takamatsu Symp. 1991. PMID: 1668890 Review.
-
Myc: a single gene controls both proliferation and apoptosis in mammalian cells.Experientia. 1996 Dec 15;52(12):1123-9. doi: 10.1007/BF01952111. Experientia. 1996. PMID: 8988255 Review.
Cited by
-
Identification of a novel proliferation-related protein, WHSC1 4a, in human gliomas.Neuro Oncol. 2008 Feb;10(1):45-51. doi: 10.1215/15228517-2007-036. Epub 2008 Jan 8. Neuro Oncol. 2008. PMID: 18182627 Free PMC article.
-
Secretion of matrix metalloproteinase-2 (72 kD gelatinase/type IV collagenase = gelatinase A) by malignant human glioma cell lines: implications for the growth and cellular invasion of the extracellular matrix.J Neurooncol. 1996 Apr;28(1):13-24. doi: 10.1007/BF00300442. J Neurooncol. 1996. PMID: 8740587
-
Myc down-regulation affects cyclin D1/cdk4 activity and induces apoptosis via Smac/Diablo pathway in an astrocytoma cell line.Cell Prolif. 2009 Feb;42(1):94-109. doi: 10.1111/j.1365-2184.2008.00576.x. Cell Prolif. 2009. PMID: 19143767 Free PMC article.
-
Histone demethylase KDM4C controls tumorigenesis of glioblastoma by epigenetically regulating p53 and c-Myc.Cell Death Dis. 2021 Jan 18;12(1):89. doi: 10.1038/s41419-020-03380-2. Cell Death Dis. 2021. PMID: 33462212 Free PMC article.
-
Analyses of human gliomas by restriction landmark genomic scanning.J Neurooncol. 1997 Nov;35(2):113-20. doi: 10.1023/a:1005712308061. J Neurooncol. 1997. PMID: 9266447
References
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Miscellaneous