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Int J Immunopathol Pharmacol ; 26(2): 393-402, 2013.
Article in English | MEDLINE | ID: mdl-23755754

ABSTRACT

In our previous study, a relationship between low expression of D2-like dopamine receptor genes and non-small cell lung cancer (NSCLC) disease was found. In this new research, by using selective agonist of these receptors, Bromocriptine (BR), we attempted to activate D2-like expression and apoptotic induction in a selective cell line of NSCLC. In addition, the relationship of apoptotic response of human lung carcinoma cells to BR and D2- dopamine receptor genes is investigated. Human lung cancer (QU-DB) cells were treated by five doses of BR at 48 h and cell viability was determined by MTT assay. The gene expression pattern of D2-like dopamine receptor Genes was studied by Real Time PCR. Nuclear morphology of cells was monitored by DAPI flourescent staining then induction of DNA fragmentation by BR was shown in an agarose gel. Finally, the detection and quantification of apoptosis and its differentiation from necrosis was carried out by using Annecxin-V-Fluos Staining. In this study, it is demonstrated that BR inhibited the proliferation of human lung cancer cells and induced apoptosis in them. In addition, the probable relationship between D2-dopamine receptor genes expression and the development of apoptosis was found. In conclusion, BR is responsible for induction of apoptosis in human lung cancer cells and can be used in treatment of these tumoric cells. In addition, normal expression of D2 dopamine receptors was associated with apoptotic effect of BR on these cells.


Subject(s)
Antineoplastic Agents/pharmacology , Apoptosis/drug effects , Bromocriptine/pharmacology , Carcinoma, Non-Small-Cell Lung/metabolism , Dopamine Agonists/pharmacology , Lung Neoplasms/metabolism , Receptors, Dopamine D2/agonists , Carcinoma, Non-Small-Cell Lung/genetics , Carcinoma, Non-Small-Cell Lung/pathology , Cell Line, Tumor , Cell Nucleus Shape/drug effects , Cell Proliferation/drug effects , Cell Survival/drug effects , Dose-Response Relationship, Drug , Gene Expression Regulation, Neoplastic , Humans , Lung Neoplasms/genetics , Lung Neoplasms/pathology , Receptors, Dopamine D2/genetics , Receptors, Dopamine D2/metabolism , Time Factors
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