GnRH Agonist Buserelin Affects Colony-Forming Efficiency of HHUA and Jurkat Cells (original) (raw)
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Life Sciences, 2002
A number of studies have demonstrated that GnRH has anti-proliferative effects on various carcinomas of breast, ovary, endometrium, prostate, pancreas, and liver origin [1 -17]. In contrast, GnRH increases the proliferative activity of lymphoid tissues and cells, which suggests that GnRH is also an important immunomodulator [18 -22]. In a previous study, we demonstrated that the colony-forming efficiencies of HHUA (derived from human endometrial carcinoma) and Jurkat (derived from human mature leukemia) cells are affected by the GnRH agonist Buserelin, and that the conditioned media of HHUA and Jurkat cells severely affect the Buserelin activity . The latter finding suggests that substances in the culture medium have some relation to the GnRH activity. Therefore, in the present study, to evaluate the effect of serum supplements on the colony-forming efficiency assay, the assay was performed using 3 lots of fetal bovine serum (FBS) and 2 lots of Nu-Serum I, a semi-synthetic serum supplement. The results showed that the colony-forming efficiencies of HHUA and Jurkat cells fluctuated greatly depending on the lot of FBS. In contrast, Buserelin significantly affected the colonyforming efficiency to similar extents in the media containing both the lots of Nu-Serum I. These results strongly suggest that the constituents of the serum supplements also influence the effect of GnRH on cell proliferation. For further studies about the relationship between substances in the culture medium and the GnRH effects on cell proliferation, it will be necessary to use a completely defined medium, and that a semi-synthetic serum supplement such as Nu-Serum I will also be useful. D
Experimental Cell Research, 1996
The possibility that human leukemic cells could syn-the in vitro growth of blast colony forming cells in culthesize growth hormone (GH) was investigated in the tured marrow obtained from children with acute HL-60 cell line. Western blot analysis of protein exlymphoblastic (ALL) and acute myelogenous leukemia tracts obtained from these cells revealed the existence (AML) [2]. Although GH is mainly synthesized by the of a major immunoreactive GH (irGH) band, with an pituitary, it has been shown that both human and rat approximate molecular weight of 22 kDa, together lymphocytes synthesize and release immunoreactive with lower amounts of 20-and 44-kDa bands. Stimulat-GH (irGH) , which seems to be important in the ing proliferating HL-60 cells with KCl clearly incontrol of their proliferation. In fact, GH synthesis creased GH concentration in the incubation medium blockade with antisense oligodeoxynucleotides to GH as compared to basal values. RT-PCR amplification of mRNA inhibits leukocyte proliferation in vitro [4], HL-60 RNA and restriction assay of the amplimers while exogenously added GH restores this effect. Taken demonstrated that those proteins were the result of together, these data suggest the possibility that a lothe expression of the GH-N (normal) gene in this cell cally produced GH may also act as a paracrine/autoline. These results were confirmed by Northern blot, crine modulator of leukemic cell proliferation. As a first which also showed that the rate of GH-N gene expresstep to assess this hypothesis, we investigated whether sion was clearly dependent upon the proliferative human leukemic cells are capable of synthesizing GH.
GnRH receptors and GnRH endocrine effects on luteoma cells
Endocrine, 1997
An ovary implanted into the spleen of an ovariectomized rat develops into a luteinized tumor, growing in response to gonadotrophins. Previously, it was shown that in vivo Buserelin, a gonadotrophin-releasing hormone (GnRH) analog, inhibited tumor growth. To determine if GnRH had a direct effect on tumor cells, the presence of GnRH receptors as well as the endocrine effects of buserelin were studied on tumoral tissue. GnRH receptors were present in luteoma in similar concentrations and dissociation constant (Kd) to control estrous ovaries. In vivo treatment with buserelin did not modify luteoma GnRH receptors. In organ incubations, luteoma secreted significantly higher estradiol and lower progesterone than estrous ovaries; addition of buserelin did not modify steroid secretion.
LH-RH and Its Antagonist Cetrorelix Inhibit Growth of Jar Human Choriocarcinoma Cells In-Vitro
International Journal of Oncology, 1995
The effects of luteinizing hormone-releasing hormone (LH-RH), and LH-RH antagonist Cetrorelix, (SB-75, [Ac-D-Nal(2)\D-Phe(4-Cl) 2 ,D-Pal(3) 3 ,D-Cit 6 ,D-Ala 10 ]LH-RH) on cell growth and the production of hCG and cAMP in JAR human choriocarcinoma cells were examined in vitro. Both LH-RH and its antagonist SB-75, at 1 \ig concentration, inhibited the growth of JAR cells in cultures. When SB-75 (1 ^.M) was given in combination with different doses (0.1 nM to 1 uM) of LH-RH, it was found that 0.1 nM LH-RH nullified the inhibitory effect of SB-75 on cell growth, however, the 100 nM and 1 uM doses of LH-RH caused a greater inhibition of cell proliferation than SB-75 alone. Incubation with LH-RH slightly increased the hCG production and the cAMP release in the cultured tumor cells. SB-75 alone or in combination with LH-RH reduced the hCG as well as the cAMP release from JAR human chorio carcinoma cells; however, the magnitude of the decrease was smaller for hCG than for cAMP. The effect of different doses of LH-RH, administered simultaneously with 1 ixM SB-75, on the cAMP production, was similar to that on cell growth: 0.1 nM LH-RH in combination with 1 p.M SB-75 caused a smaller inhibition of cAMP than SB-75 alone. However,
Effect of inhibitors of plant cell division on mammalian tumor cells in vitro
Cancer Research, 1981
We studied the activity of 14 compounds, all of which have been shown to interfere in plant cell division, in two animal tumor cell cultures, EL-4 and L1210. Four compounds [propham, chlorpropham, bensulide S-(O,O-diisopropylphosphorodithioate) ester of A/-(2-mercaptoethyl)benzenesulfonamide), and siduron] had a 50% inhibitory dose less than 10~4 M; six [2,3,5-triiodobenzoic acid, (2,4-dichlorophenoxy)acetic acid, bromacil, (2,4,5-trichlorophenoxy)acetic acid, naptalam, and (4-chloro-2-methylphenoxy)acetic acid] had a 50% inhibitory dose between 10~" and 10~3 M, and the remaining four 2,3: 4,6-di-O-isopropylidene-2-keto-L-gulonate, eptam, maleic hydrazide, and 4-(methylsulfonyl)-2,6-dinitro-/\/,N,-dipropylaniline] had a 50% inhibitory dose at higher than 10~3 M. There was a significant correlation between the effect on the two cell lines as well as between the inhibition of cell proliferation and that of thymidine and leucine uptake. More detailed study of cell proliferation and leucine and thymidine uptake for bensu lide and 2,3,5-triiodobenzoic acid revealed a dose-response pattern of inhibition starting shortly after exposure of the cells to the compounds. These results indicate that some inhibitors of plant cell division are capable of inhibiting the proliferation of animal tumor cells.
Regulatory mechanism of cell division
Experimental Cell Research, 1973
Experiments were carried out to study the induction of endoreduplication by colchicine in Chinese hamster cells cultivated in vitro. The cells that endoreduplicate are those that. at the moment of treatment, are in late-S and, in particular, in G2. The endoreduplication cycle consists of twc periods of synthesis (S 1 and S2), as already noted by Schwarzacher & Schnedl [42], separated by an intervening period that we call G? The S2 synthesis begins in a highly synchronous manner, without the cells having gone into a c-mitosis. The quantity of endoreduplicated cells induced is proportional to the 3.5th root of the colchicine concentration, above a threshold value, and does not depend on the duration of the treatment. When the cultures are treated twice with colchicine, the second treatment is also able to induce endoreduplication and, after it, there appear double endoreduplicated cells (with quadruplochromosomes).
Journal of Histochemistry & Cytochemistry, 1986
The ability to measure cell proliferation is important in the study of cancer biology. The usual technique for quantitating proliferating cells in tissue explant and organ culture by detection of [3H]-thymidine incorporation into DNA by autoradiography is tedious and time-consuming. We have developed a technique for identification and quantitation of bromodeoxyuridine (an analogue of thymidine) in cultured tissue explants. Fetal mouse colon explants were exposed in vitro to bromodeoxyuridine (BUdR) or [3H]-thymidine for 3 to 72 hr and then for various periods to unlabeled thymidine. The tissues were stained with a monoclonal anti-bromodeoxyuridine antibody and in parallel [3H]-thymidine incorporation was detected by autoradiography. Incorporation of BUdR was measured by quantitating the amount of pigment deposited over nuclei after immunohistochemical staining, using an optical data digitizer. It was found that both techniques identified proliferating cells. Dividing cells were pres...