Differences of Cell Growth and Cell Cycle Regulators Induced by Basic Fibroblast Growth Factor Between Nifedipine Responders and Non-responders

Abstract

Abstract. Differences of cell proliferation, cell cycle, and G 1 / S transition regulatory proteins of gingival fibroblasts derived from nifedipine-reactive patient (NIFr) and nifedipine-nonreactive patient (NIFn) in the presence of basic fibroblast growth factor (bFGF) were investigated to elucidate the mechanism of gingival overgrowth associated with nifedipine, one of the Ca

SOCS-3 antagonises the proliferative and migratory effects of fibroblast growth factor-2 in prostate cancer by inhibition of p44/p42 MAPK signalling

“…We could thus extend the results of a previous work, in which it was revealed that FGF-2 increases the expression and secretion of heparin affin regulatory peptide/ pleiotrophin, cellular proliferation and migration (Hatziapostolou et al 2006). One could hypothesise that expression of FGF-2 targets such as cyclin E, retinoblastoma or matrix metalloproteinases is affected through the effect of SOCS-3 on p44/p42 MAPK phosphorylation (Muddasani et al 2007, Takeuchi et al 2007. We demonstrate for the first time that SOCS-3 may interfere with oncogenic events caused by the p44/p42 MAPK pathway in cancer.…”

Drug-induced gingival overgrowth and its tentative pharmacotherapy

“…In case of bFGF, the elevations of pRB (Ser780), RB, and cyclin A protein levels in NIFr cells did not differ from those of NIFn cells, but pRB(ser780) in case of IGF-I. The growth of NIFr cells was greater than NIFn cells as a result of the active G 1 /S transition of NIFr cells, by the increments of cyclin E, pCDK2 and pRB (ser807/811) protein in NIFr cells [17,18] (Fig. 1).…”

“…2 [18]. NIF inhibits phosphodiesterase to increase protein kinase G, and then activates p38 mitogen-activated protein kinase (p38 MAPK) and activating transcription factor-2, resulting in apoptosis and inhibition of cell growth.…”

“…When RB binds E2F at G 1 phase, expression of the target gene is suppressed. At late G 1 , RB is phosphorylated forming pRB by cyclin D-CDK4/6, and then by cyclin E-CDK 2 and cyclin A-CDK2, leading to the release of E2F from RB [18]. In NIFr cells, pRB (ser807/811) is phosphorylated through cyclin E-CDK2.…”

“…The major water-soluble constituent of licorice is glycyrrhizin, which is known to be partly hydrolyzed by glucuronidase to its aglycone glycyrrhetinic acid which exists in 18 alpha (18a-GA) and 18 beta stereoisomeric forms [34]. 18a-GA has a variety of interesting activities such as the growth-promoting [18]). In this occasion, NIFn cells were more active than NIFr cells, indicating NIFn cells were depressed cell growth by nifedipine, as well as NIFn cells undergo apoptosis by nifedipine.…”