The in vitro influence of eight hormones and growth factors on the proliferation of eight sarcoma cell lines

Abstract

Little is known about the regulation of sarcoma proliferation by hormones and/or growth factors. We therefore characterised the in vitro proliferative influence on eight sarcoma cell lines of the platelet-derived growth factor, the insulin-like growth factor 1, triiodothyronine, the epidermal growth factor, the luteinising-hormone-releasing hormone, progesterone, gastrin and 17 beta-oestradiol. The influence of the different factors on the proliferation of sarcoma cell lines was measured by the colorimetric 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide test. Two culture media were studied: (1) a nutritionally poor medium containing 2% of fetal calf serum and (2) a nutritionally rich one containing 5% or 10% FCS both with and without the addition of non-essential amino acids. The results were analysed either by conventional statistical analyses or by a classification method based on a decision-tree approach developed in Machine Learning. This latter method was also compared to other classifiers (such as logistic regression and k nearest neighbours) with respect to its accuracy of classification. Monovariate statistical analysis showed that each of the eight cell lines exhibited sensitivity to at least one factor, and each factor significantly modified the proliferation of five or six of the eight cell lines under study. Of these eight lines one of fibrosarcoma origin was the most "factor-sensitive". Decision-tree-related data analysis enabled the specific pattern of factor sensitivity to be characterised for the three histological types of cell line under study. The effects of hormone and growth factors are significantly influenced by the type of culture medium used. The method used appeared to be an accurate classifier for the kind of data analysed. Sarcoma proliferation can be modulated, at least in vitro, by various hormones and growth factors, and the proliferation of each histopathological type exhibited a distinct sensitivity to different hormone and/or growth-factors.

In vitro influence of lectins and neoglycoconjugates on the growth of three human sarcoma cell lines

“…They were the Hs 729 (ATCC HTB-153), of rhabdomyosarcomatous origin, the SK-UT-1 (ATCC HTB-114) (Fogh et al 1977) and the SK-LMS-1 (ATCC HTB-88) (Fogh et al 1977), the latter two of which were of leiomyosarcomatous origin. The cell lines were cultured as previously described Remmelink et al 1998). Brie¯y, they were cultured as monolayers at a temperature of 37°C in an atmosphere containing 5% CO 2 in closed Falcon plastic dishes (Nunc, Poly Labo, Strasbourg, France) .…”

“…Little is known about the factors regulating the growth of these tumours (Remmelink et al 1998). Growth regulation can be triggered by protein/carbohydrate interaction, which is known to in¯uence the activity of diverse intracellular signalling pathways (Villalobo et al 1997).…”

mTORC1 Signaling Can Regulate Growth Factor Activation of p44/42 Mitogen-activated Protein Kinases through Protein Phosphatase 2A

“…In vitro, mTORC1 phosphorylates at least two residues (Thr 37 and Thr 46 ) of 4E-BP1 (3,22,23). Direct phosphorylation of S6K1 has also been reported (24).…”

“…Although previously it had been shown that in NIH3T3 cells rapamycin does not inhibit activation of MAPKs (2), there are anecdotal reports that rapamycin can influence activation of MAPK pathways (36). We were interested in the possible role of mTORC1 in coordinating both translational initiation and MAPK activation after stimulation by growth factors reported to be mitogenic in sarcoma cells (37)(38)(39)(40). Cell Lines and Growth Conditions-Culture conditions in serum-containing and serum-free, antibiotic-free media have been described for the human cell lines previously (40,41).…”

Preclinical Mouse Models of Neurofibromatosis

“…Many of these tumors are high-grade osteosarcomas or malignant fibrous histiocytomas that have a poor prognosis (Huvos et al, 1985;Inwards and Unni, 1995;Laskin et al, 1988;Murray et al, 1999). Although TP53 inactivation is common in RAD-induced sarcomas (Brachman et al, 1991;Nakanishi et al, 1998), the other molecular lesions are largely unknown (Beech et al, 1998;Cowan et al, 1990;Remmelink et al, 1998;Sekyi-Otu et al, 1995;Wang et al, 1994). MPNST, the most common sarcoma that arises de novo in persons with NF1, has also been reported as a SMN (Li et al, 2002).…”