Caveolin-1 expression is maintained in rat and human astroglioma cell lines

被引:31
作者
Cameron, PL [1 ]
Liu, CD [1 ]
Smart, DK [1 ]
Hantus, ST [1 ]
Fick, JR [1 ]
Cameron, RS [1 ]
机构
[1] Med Coll Georgia, Program Neurobiol, Inst Mol Med & Genet, Augusta, GA 30912 USA
关键词
caveolae; astroglial cells; astrogliomas; nervous system proteins;
D O I
10.1002/glia.10036
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Caveolin-1 is the principal structural and functional component of caveolae, a plasmalemmal compartment that has been proposed to sequester lipid and protein components that participate in transmembrane signal transduction processes. Multiple studies reveal a reduction in the expression level of caveolin-1 mRNA and protein in many carcinomas as well as transformed cells. The human caveolin-1 gene is localized to a suspected tumor suppressor locus (7q31.1). Collectively, these data have been taken to imply that caveolin-1 may function in a tumor suppressor capacity. To determine if a reduction in the expression level of caveolin-1 mRNA and protein accompanied the transformation of astrocytes, we undertook studies of two transformed rat astroglial cell lines, C6 and DI TNC1, as well as several cell lines derived from human glioblastoma tumors: T98G, U87MG, U118MG, U138MG, and U373MG. Ultrastructural, immunolocalization, immunoblot, and Northern blot analyses demonstrated that caveolin-1 message and protein were expressed in all rat and human glioma cells. The localization pattern, buoyant density, and detergent-insolubility property of caveolin-1 protein were indistinguishable from that determined for nontransformed type 1 astrocytes in culture. Nucleotide sequence analyses of caveolin-1 cDNAs indicate that mutations are not present in the caveolin-1 sequence in any of the glioma cell types. Taken together with previous analyses, these data indicate that, at least for astrocytes, the process of transformation in and of itself is not solely sufficient to reduce the level of caveolin-1 expression, and that caveolin-1 expression in and of itself is not solely sufficient to prevent the acquisition of a transformed phenotype. (C) 2002 Wiley-Liss, Inc.
引用
收藏
页码:275 / 290
页数:16
相关论文
共 68 条
[1]   The p53 network [J].
Agarwal, ML ;
Taylor, WR ;
Chernov, MV ;
Chernova, OB ;
Stark, GR .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (01) :1-4
[2]   The caveolae membrane system [J].
Anderson, RGW .
ANNUAL REVIEW OF BIOCHEMISTRY, 1998, 67 :199-225
[3]   NEGATIVE EFFECTS OF WILD-TYPE P53 AND S-MYC ON CELLULAR GROWTH AND TUMORIGENICITY OF GLIOMA-CELLS - IMPLICATION OF THE TUMOR-SUPPRESSOR GENES FOR GENE-THERAPY [J].
ASAI, A ;
MIYAGI, Y ;
SUGIYAMA, A ;
GAMANUMA, M ;
ILHONG, S ;
TAKAMOTO, S ;
NOMURA, K ;
MATSUTANI, M ;
TAKAKURA, K ;
KUCHINO, Y .
JOURNAL OF NEURO-ONCOLOGY, 1994, 19 (03) :259-268
[4]   Downmodulation of caveolin-1 expression in human ovarian carcinoma is directly related to α-folate receptor overexpression [J].
Bagnoli, M ;
Tomassetti, A ;
Figini, M ;
Flati, S ;
Dolo, V ;
Canevari, S ;
Miotti, S .
ONCOGENE, 2000, 19 (41) :4754-4763
[5]   DIFFERENTIATED RAT GLIAL CELL STRAIN IN TISSUE CULTURE [J].
BENDA, P ;
LIGHTBODY, J ;
SATO, G ;
LEVINE, L ;
SWEET, W .
SCIENCE, 1968, 161 (3839) :370-+
[6]  
Bender FC, 2000, CANCER RES, V60, P5870
[7]   HETEROGENEITY OF GENOTYPIC AND PHENOTYPIC CHARACTERISTICS OF 15 PERMANENT CELL-LINES DERIVED FROM HUMAN GLIOMAS [J].
BIGNER, DD ;
BIGNER, SH ;
PONTEN, J ;
WESTERMARK, B ;
MAHALEY, MS ;
RUOSLAHTI, E ;
HERSCHMAN, H ;
ENG, LF ;
WIKSTRAND, CJ .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1981, 40 (03) :201-229
[8]  
BIGNER SH, 1990, CANCER RES, V50, P8017
[9]   p53 regulates caveolin gene transcription, cell cholesterol, and growth by a novel mechanism [J].
Bist, A ;
Fielding, CJ ;
Fielding, PE .
BIOCHEMISTRY, 2000, 39 (08) :1966-1972
[10]  
Bögler O, 1999, CELL GROWTH DIFFER, V10, P73