Coordinate oncodevelopmental modulation of alternative splicing of fibronectin pre-messenger RNA at ED-A, ED-B, and CS1 regions in human liver tumors

The molecular diversity of fibronectin arises from alternative RNA splicing at regions termed ED-A, ED-B, and IIICS. We investigated the splicing patterns of fibronectin pre-mRNA at both ED-B and IIICS regions in various human liver tissues with an emphasis on the expression of the alternative cell...

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Bibliographic Details
Published in:Cancer research (Chicago, Ill.) Ill.), 1993-05, Vol.53 (9), p.2005-2011
Main Authors: OYAMA, F, HIROHASHI, S, SAKAMOTO, M, TITANI, K, SEKIGUCHI, K
Format: Article
Language:English
Subjects:
Alternative Splicing
Amyloid beta-Protein Precursor - genetics
Base Sequence
Biological and medical sciences
Fibronectins - chemistry
Fibronectins - genetics
Gastroenterology. Liver. Pancreas. Abdomen
Gene Expression
Humans
Kininogens - genetics
Liver - embryology
Liver Diseases - genetics
Liver Neoplasms - genetics
Liver. Biliary tract. Portal circulation. Exocrine pancreas
Medical sciences
Molecular Sequence Data
Oligodeoxyribonucleotides - chemistry
RNA, Messenger - genetics
RNA, Neoplasm - genetics
Tumors
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Summary:The molecular diversity of fibronectin arises from alternative RNA splicing at regions termed ED-A, ED-B, and IIICS. We investigated the splicing patterns of fibronectin pre-mRNA at both ED-B and IIICS regions in various human liver tissues with an emphasis on the expression of the alternative cell adhesive site CS1 within the IIICS region. The relative abundance of the fibronectin mRNA containing the CS1 sequence was significantly increased in both fetal and cancerous liver tissues, although it was not affected in nonmalignant tissues with chronic hepatitis and cirrhosis. Similarly, the relative abundance of the fibronectin mRNA containing the ED-B region was also increased in both fetal liver and liver tumors, showing a close parallelism with the splicing pattern at the ED-A region. Immunohistochemical examination of cancerous liver tissues with monoclonal antibodies directed to the ED-A and ED-B segments revealed that the fibronectin isoforms containing these extra peptide segments were specifically deposited in the tumor nodules. Other genes encoding kininogen, gamma chain of fibrinogen, and beta-amyloid protein precursor, all of which had been shown to be alternatively processed, did not show any significant alteration in the splicing pattern in cancerous liver tissues. These results indicate that the alternative splicing of fibronectin pre-mRNA at the ED-A, ED-B, and IIICS regions is coordinately modulated in both fetal and cancerous liver tissues toward inclusion of the extra peptide segments and that not all but only selected genes are susceptible for "fine tuning" of alternative RNA splicing in cancerous liver tissues.
ISSN:0008-5472
1538-7445