Antisense expression of protein kinase C alpha improved sensitivity to anticancer drugs in human lung cancer LTEPa-2 cells
Abstract
AIM: To study the role of protein kinase C alpha (PKC alpha) in sensitivity to some clinical anticancer drugs in human lung cancer LTEPa-2 cells.
METHODS: Human lung cancer cell model expressing antisense PKC alpha was established and characterized by gene transfection and immunoblotting. Northern blotting was used to analyze the expression of multiple drug resistance (mdr-1) gene and antisense PKC alpha mRNA. IC50 for some anticancer drugs in cultured cells were measured.
RESULTS: Expression of antisense PKC alpha mRNA inhibited mdr-1 gene expression in lung cancer cells and improved sensitivity to anticancer drugs (harringtonine, carboplatin, bleomycin A5, vincristine and doxorubicin) in lung cancer cells. IC50 for harringtonine, carboplatin, bleomycin A5, vincristine, and doxorubicin was decreased by 46.4%, 42.1%, 79%, 69.9%, and 61.6% respectively. CONCLUSION: PKC alpha plays an important regulation role of mdr-1 gene expression and drug sensitivity in human lung cancer cells.
Keywords:
METHODS: Human lung cancer cell model expressing antisense PKC alpha was established and characterized by gene transfection and immunoblotting. Northern blotting was used to analyze the expression of multiple drug resistance (mdr-1) gene and antisense PKC alpha mRNA. IC50 for some anticancer drugs in cultured cells were measured.
RESULTS: Expression of antisense PKC alpha mRNA inhibited mdr-1 gene expression in lung cancer cells and improved sensitivity to anticancer drugs (harringtonine, carboplatin, bleomycin A5, vincristine and doxorubicin) in lung cancer cells. IC50 for harringtonine, carboplatin, bleomycin A5, vincristine, and doxorubicin was decreased by 46.4%, 42.1%, 79%, 69.9%, and 61.6% respectively. CONCLUSION: PKC alpha plays an important regulation role of mdr-1 gene expression and drug sensitivity in human lung cancer cells.