K-FGF mediated transformation and induction of metastatic potential involves altered ornithine decarboxylase and S-adenosylmethionine decarboxylase expression - role in cellular invasion

Ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase (SAMDC) expression was investigated in NIH-3T3 fibroblasts that secrete K-FGF. Correlations between altered ODC and SAMDC expression and malignant potential were determined. Increased ODC and SAMDC expression was associated with increased expression of both ODC and SAMDC mRNA and enzyme activity levels. Transcriptional and post-transcriptional regulatory mechanisms were found to account for the increased expression of both ODC and SAMDC. Amplification of the ODC gene also played a role. Correlations between the expression of ODC and the invasion ability of the K-FGF overexpressing cells were also found. Additionally, putrescine, which is a cellular polyamine, was found to play a role in determining the nature of the invasive capacity of the K-FGF overexpressing cells. The results of this study which established correlations between alterations in the expression of ODC and SAMDC, the key rate limiting and regulatory activities in the synthesis of cellular polyamines, and malignant potential as a consequence of K-FGF overexpression supports a model which suggests that growth factor modulation of ODC and SAMDC expression is part of the altered growth regulatory program associated with cellular transformation and malignant progression.PT: J; CR: ASHIDA Y, 1992, CANCER RES, V52, P5313 AUVINEN M, 1992, NATURE, V360, P355 AUVINEN M, 1997, J NATL CANCER I, V89, P533 DAMEN JE, 1991, BIOCHIM BIOPHYS ACTA, V1097, P103 DEBUSTROS A, 1985, J BIOL CHEM, V260, P98 DELLIBOVI P, 1988, MOL CELL BIOL, V8, P2933 EGAN SE, 1990, ANTICANCER RES, V10, P1341 HEBY O, 1990, TRENDS BIOCHEM SCI, V15, P153 HOVIS JG, 1986, J BIOL CHEM, V261, P10380 HUANG AP, 1994, EXP CELL RES, V213, P335 HURTA RAR, 1990, BIOCHEM BIOPH RES CO, V167, P258 HURTA RAR, 1993, J CELL PHYSIOL, V156, P272 HURTA RAR, 1994, J CELL PHYSIOL, V161, P383 HURTA RAR, 1996, J CELL BIOCHEM, V60, P572 KAHANA C, 1985, J BIOL CHEM, V260, P15390 KAMINSKA B, 1992, FEBS LETT, V304, P198 KONTULA KK, 1984, P NATL ACAD SCI USA, V81, P731 KUBOTA S, 1995, BIOCHEM BIOPH RES CO, V208, P1106 KUBOTA S, 1997, J NATL CANCER I, V89, P567 MANNI A, 1995, CANCER LETT, V95, P23 PATEL AR, 1998, AM J PHYSIOL-CELL PH, V275, C590 PEGG AE, 1988, CANCER RES, V48, P759 PEGG AE, 1992, PHARMACOL THERAPEUT, V56, P359 PERSSON L, 1985, BIOCHEM BIOPH RES CO, V131, P239 RAY R, 1999, AM J PHYSIOL, C684 SERTICH GJ, 1987, BIOCHEM BIOPH RES CO, V143, P424 TABIB A, 1998, INT J BIOCHEM CELL B, V30, P135 TABIB A, 1999, INT J BIOCHEM CELL B, V31, P12899 TAYLOR WR, 1993, EXP CELL RES, V204, P295 THEILLET C, 1989, ONCOGENE, V4, P915 TIESMAN J, 1989, IN VITRO CELL DEV B, V25, P1193 WALLON UM, 1994, MOL CARCINOGEN, V11, P138 WANG JY, 1992, AM J PHYSIOL, G494 WRIGHT JA, 1990, ANTICANCER RES, V10, P1247 WRIGHT JA, 1993, CRIT REV ONCOGENESIS, V4, P473 YOSHIDA MC, 1988, P NATL ACAD SCI USA, V85, P4861; NR: 36; TC: 1; J9: MOL CELL BIOCHEM; PG: 8; GA: 552TCSource type: Electronic(1