ISSN:
0730-2312
Schlagwort(e):
squamous cell carcinoma
;
differential display
;
tropomyosin α
;
cytokine KC
;
ribosomal protein L18a
;
antigen Sp17
;
Life and Medical Sciences
;
Cell & Developmental Biology
Quelle:
Wiley InterScience Backfile Collection 1832-2000
Thema:
Biologie
,
Chemie und Pharmazie
,
Medizin
Notizen:
Molecular changes occurring with tumor formation and metastasis need to be identified in order to define novel markers and targets for chemoprevention and therapy. Cell lines from a multistage model of murine squamous cell carcinoma were analyzed for differences in gene expression using mRNA differential display. mRNA was isolated from primary keratinocytes, an in vitro transformed keratinocyte line (Pam 212), and three metastatic cell lines derived from Pam 212 following tumor progression in vivo. cDNA was synthesized by reverse transcription and amplified by PCR using 72 primer combinations to screen and compare approximately 3,600 sequences. Five cDNAs with a differential expression pattern confirmed by Northern blot analysis were cloned and sequenced, revealing homology with known genes. The gene encoding tropomyosin α was preferentially expressed in primary keratinocytes; genes for tyrosine kinase Yes-associated protein (YAP65) and ribosomal protein L18a were preferentially expressed in transformed and metastatic tumor cell lines; and genes for the Gro-α family cytokine KC and antigen Sp17 exhibited increased expression in the three metastatic cell lines. The structure and function of the genes identified suggest that they may possibly be linked to cell shape and motility, signal transduction, protein synthesis, growth, granulocyte chemotaxis, and angiogenesis. This study demonstrates the ability of mRNA differential display to detect altered gene expression in this tumor progression model of murine squamous cell carcinoma, and the potential usefulness of this approach for identification of candidate genes as chemoprevention markers and targets. J. Cell. Biochem. Suppls. 28/29:90-100. Published 1998 Wiley-Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
Zusätzliches Material:
3 Ill.
Materialart:
Digitale Medien
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