calcimycin and Laryngeal-Neoplasms

To study the effects of A23187 on intracellular free Ca2+ concentration and apoptosis on human squamous cell carcinoma of larynx.. Human squamous cell carcinoma of larynx were randomly divided into 4 groups ( 3 treated with A23187 groups and 1 control). Intracellular free Ca2+ was measured by using the fluorescence Ca2+ indicator Fura-2/AM; Apoptotic rate was measured by using FACS 420 Flow Cytometer; DNA gel electrophoresis at different time points.. Intracellular [Ca2+]i at 5 h, 24 h, 48 h after A23187 exposure were (123.48+/-21.54) mmol/L, (110.54+/-11.32) mmol/L, (88.63+/-9.95) mmol/L and all were higher than control group (54.23+/-8.73) nmol/L (P <0.01); Apoptotic rate in 5, 24, 48 h were (3.84+/-1.12), (7.65+/-1.35), (9.49+/-1.31) and also higher than control group (2.63+/-0.75) (P < 0.01) and increased with time prolonged.. Exposuring to A23187 would interfere with intracellular free Ca2+ concentration and apoptotic rate in human squamous cell carcinoma of larynx suggests that there may be certain relation between them.

Topics: Apoptosis; Calcimycin; Calcium; Cell Line, Tumor; Humans; Ionophores; Laryngeal Neoplasms

The regulation of IL-6 mRNA expression was studied in human blood monocytes and in the human epidermoid carcinoma cell line HEp-2. In human monocytes phorbol-12-myristate 13-acetate (PMA) did not induce IL-6 but it increased IL-1 beta and IL-8 mRNA levels. Furthermore, in monocytes, protein kinase C (PKC) activation by PMA even reduced IL-1-induced IL-6 mRNA, and IL-1-induced IL-6 synthesis was increased by the PKC inhibitor staurosporine. IL-6 synthesis in HEp-2 cells was induced by IL-1, PMA, and calcium ionophore A 23187 but not by dibutyryl-cAMP. PMA-, but not IL-1-induced IL-6 synthesis in HEp-2 cells was inhibited by staurosporine. PMA pretreatment of HEp-2 cells abolished PMA-induced IL-6 but the IL-1 effect was not reduced. These data indicate that IL-6 can be induced by a PKC-independent pathway in monocytes and HEp-2 cells. In monocytes PKC activation does not induce IL-6 and PMA interferes with the IL-1 effect. Transcription factors known to be involved with the regulation of IL-6 expression were studied by gel retardation assays. NF-IL-6 and AP-1 activity were constitutively expressed in monocytes and HEp-2 cells under conditions where IL-6 mRNA was not detectable and levels did not change in response to stimulation by IL-1 or PMA. In contrast, NF-kB was increased by both IL-1 and PMA, but only the effect of PMA, and not that of IL-1, was inhibited by staurosporine. In summary, these results show tissue-specific differences in the regulation of IL-6 expression. Induction of IL-6 in monocytes is PKC independent. In the epithelial cell line HEp-2 IL-6 is inducible by PKC as well as by a PKC-independent pathway.

Topics: Alkaloids; Base Sequence; Calcimycin; Carcinoma, Squamous Cell; DNA-Binding Proteins; Gene Expression Regulation; Interleukin-1; Interleukin-6; Laryngeal Neoplasms; Lipopolysaccharides; Molecular Sequence Data; Monocytes; NF-kappa B; Organ Specificity; Polymerase Chain Reaction; Protein Kinase C; Signal Transduction; Staurosporine; Tetradecanoylphorbol Acetate; Transcription Factors; Tumor Cells, Cultured