Cell lines derived from the major morphological types of human lung cancer were tested for their ability to utilize the SV40 enhancerlearly promoter. These cell lines were transfected with a recombinant plasmid containing a reporter gene, coding for chloramphenicol acetyltransferase (CAT), under the
Intron/Exon organization and polymorphisms of the PLK3/PRK gene in human lung carcinoma cell lines
β Scribed by Jonathan Wiest; Adam M. Clark; Wei Dai
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- English
- Weight
- 127 KB
- Volume
- 32
- Category
- Article
- ISSN
- 1045-2257
- DOI
- 10.1002/gcc.1204
No coin nor oath required. For personal study only.
β¦ Synopsis
Abstract
PLK3/PRK, a conserved polo family protein serine/threonine kinase, plays a significant role at the onset of mitosis and mitotic progression. Recently, PLK3/PRK has been shown to induce apoptosis when overexpressed in cell lines and is also implicated in cell proliferation and tumor development. Forty lung tumor cell lines were used for singleβstrand confirmation polymorphism (SSCP) analysis and DNA sequencing to examine the mutational status of PLK3/PRK. No missense or nonsense mutations were revealed in the lung carcinoma cell lines examined. However, three polymorphisms were identified as: a G to A at position 720, an A to G at 1053, and a G to C at 1275. Intron/exon boundaries were determined by amplification of genomic DNA with PLK3/PRK exonβspecific primers. The amplification products with increased size relative to the cDNA were sequenced. Fifteen exons throughout the open reading frame were characterized. None of the introns were exceptionally large, typically ranging from 100β300 basepairs in length. These results suggest that although PLK3/PRK expression is downregulated in a majority of lung carcinoma samples, mutational inactivation of the coding sequence of the PLK3/PRK gene appears to be a rare event in lung cancer. Β© 2001 WileyβLiss, Inc.
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