Objective:To study the change of the physiological characteristic of lung cancer SPC-A1 after its mtDNA transcriptpromoter was blocked by antisense peptide nucleic acid(asPNA).Methods:asPNA to the transcript promoter region on the heavychain of mtDNA was synthesized

then asPNA-triphenyl phosphate complex was constructed and identified.This complex wastransfected into SPC-A1.laser confocal microscope was used to detect the location of asPNA-triphenyl phosphate complex inSPC-A1.At 48 h behind transfection

the transcription of the gene encoded by mtDNA was detected by RT-PCR.Cell cycle andapoptosis/necrosis of SPC-A1 were detected by flow cytometry.The concentration of ATP in SPC-A1 was examined by spontaneousfluorescence analyzer.All of those results were compared with those of untransfected SPC-A1.Results:asPNA-triphenyl phosphatecomplex was successfully obtained.Confocal laser scanning microscope discovered that antisense peptide nucleic acid-triphenylphosphate complex had been successfully transfected into the mitochondrion of SPC-A1.The transcriptional level of the gene encodedby mtDNA and concentration of ATP in the transfected SPC-A1 were lower significantly than the untransfected SPC-A1(P<0.01).Theanalysis of Cell cycle displayed that noticeable sbu-G1 peak appeared in the transfected group.Annexin Ⅴ-PI double labelingconfirmed the apoptosis rate of lung cancer cell in the transfected group significantly increased.Conclusion:Carried by electronicshift lipophilic cation-triphenyl phosphate

asPNA can enter the mitochondrion of SPC-A1 and block the transcript of gene encoded bymtDNA to impact the synthesis of energy and induce apoptosis of SPC-A1.