Premium
Retinoic acid and 1,25‐dihydroxyvitamin D 3 inhibit tenascin‐C expression in rat glioma C6 cells
Author(s) -
AlvarezDolado Manuel,
GonzálezSancho José Manuel,
NavarroYubero Cristina,
GarcíaFernández Luis F.,
Muñoz Alberto
Publication year - 1999
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19991015)58:2<293::aid-jnr9>3.0.co;2-h
Subject(s) - retinoic acid , glioma , tenascin c , downregulation and upregulation , angiogenesis , cancer research , cytotoxic t cell , carcinogenesis , chemistry , biology , extracellular matrix , microbiology and biotechnology , biochemistry , in vitro , gene
Tenascin‐C (Tn‐C) is an extracellular matrix protein with growth‐, invasive‐, and angiogenesis‐promoting activities. Tn‐C is upregulated during wound healing, tumorigenesis, and other pathological conditions. Highly malignant gliomas with poor prognosis exhibit high levels of Tn‐C expression. Here we demonstrate that Tn‐C RNA expression in glioma C6 cells is inhibited in a dose‐dependent manner by retinoic acid (RA) and 1,25‐dihydroxyvitamin D 3 (1,25‐D 3 ). No additive or synergistic effects were found. Inhibition is maximum 24 hr after RA or 1,25‐D 3 treatment, prior to a delayed cytotoxic effect starting at day 4–5 of treatment, and correlates with a reduction in the synthesis of Tn‐C protein. Tn‐C expression is also inhibited, but to a lesser extent by prostaglandin D2 (PGD2). Furthermore, both RA and 1,25‐D 3 , but not PGD2 abolish the induction of Tn‐C by the tumor promoter 12‐O‐tetradecanoyl phorbol 13‐acetate. The inhibition of Tn‐C expression might be relevant for the anti‐cancer activity of RA and 1,25‐D 3 .J. Neurosci. Res. 58:293–300, 1999. © 1999 Wiley‐Liss, Inc.