ABSTRACT
Objective To study the effects of P53, PCNA, Bcl-2 protein and their relationship in salivary adenoid cystic carcinoma(SACC). Methods These proteins were examined by immunohistochemistry. Results Overexpressions of P53 and PCNA were revealed in ACC samples, they were higher than those in (polymorphous adenomas) PA, but expression of Bcl-2 protein was not different between ACC and PA. In 3 subtypes of ACC, expressions of 3 proteins were different. Conclusion Mutations of P53, Bcl-2 may be involed in the occurrence of SACC, expression of PCNA and mutation of P53 may coexist in the development of the SACC.
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Objective: To study the significance of intracellular free calcium levels ([Ca 2+]i) and protein kinase C(PKC) levels in the process of human salivary gland mucoepidermoid carcinoma MEC-1 cell apoptosis induced by adriamycin. Methods: MEC-1 cells were treated with adriamycin at 10 ?mol/L for 30 s～24 h.Apoptosis of the cells was investigated by light and electron microscopy, agarose gel electrophoresis and flow cytometry. [Ca 2+]i was determined by flow cytomerty, PKC by Bardford method. Results: The results showed that MEC-1 cells presented classic morphologic features of apoptosis. [Ca 2+]i in the treated cells was increased from (36.63?0.61) nmol/L to (84.00?0.45) nmol/L after 30 s～24 h treatment,while that in the control cells was 17.43?0.47 (P
ABSTRACT
Objective To explore whether or not driamycin inhibits mEC cells by apoptosis. MethodsAdriamycin was used for mucoepidermoid carcinoma cells mEC-l. Morphologic changes were observed atdifferent times by light and electronic microscope. DNA fragments were shown on agarose gelelectrophoresis. DNA content and cell cycles were analyzed by flow cytometer. Changes of intracellularcalcium ion was monitored by flow cytometer. Results mEC-1 cells presented with classic morphologicfeatures of apoptosis. Intracellular calcium ion was increased. Conclusion Apoptosis followed by thechanges of intracellular calcium ion in human salivary gland mucoepidermoid carcinoma cells is one of themechanisms of adriamycin inhibited tumor cell growth.