[Effect of antisense oligodeoxynucleotides of RNA component of human telomerase on cisplatin induced apoptosis in K562 cells].
Yang Xiao, Huan Zhang
Abstract
Yang Xiao, Huan Zhang
Abstract
OBJECTIVE: To research whether the antisense oligodeoxynucleotide (ASODN) of RNA component of human telomerase (hTR) can increase the susceptibility of K562 cells to cisplatin. METHODS: K562 cells were treated with phosphorothoate ASODN complementary to the template region of hTR in vivo. The changing of telomerase activity was assayed by TRAP-PCR-ELISA and apoptosis by DNA gel electrophoresis, Annexin V, flow cytometry. RESULTS: There was a marked decrease in telomerase activity in ASODN treated cells as compared with that in control and sense oligodeoxynucleotide (SODN)-treated cells; but no difference between the latter two groups. Agarose gel electrophoresis of genomic DNA from K562 cells treated with ASODN and cisplatin combination for 72 h showed typical DNA ladder; neither did DNA ladder from K562 cells treated with SODN plus cisplatin nor cisplatin alone. Apoptosis rates of K562 cells treated with ASODN for 24 h and then with cisplatin for 72 h were significantly increased. There were statistically significant difference in the percentage of apoptotic cells between hTR ASODN plus cisplatin and SODN plus cisplatin or cisplatin alone group. CONCLUSION: ASODN complementary to the template region of hTR can significantly suppress the telomerase activity and enhance cisplatin-induced apoptosis of K562 cells in vivo.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
OBJECTIVE: To research whether the antisense oligodeoxynucleotide (ASODN) of RNA component of human telomerase (hTR) can increase the susceptibility of K562 cells to cisplatin. METHODS: K562 cells were treated with phosphorothoate ASODN complementary to the template region of hTR in vivo. The changing of telomerase activity was assayed by TRAP-PCR-ELISA and apoptosis by DNA gel electrophoresis, Annexin V, flow cytometry. RESULTS: There was a marked decrease in telomerase activity in ASODN treated cells as compared with that in control and sense oligodeoxynucleotide (SODN)-treated cells; but no difference between the latter two groups. Agarose gel electrophoresis of genomic DNA from K562 cells treated with ASODN and cisplatin combination for 72 h showed typical DNA ladder; neither did DNA ladder from K562 cells treated with SODN plus cisplatin nor cisplatin alone. Apoptosis rates of K562 cells treated with ASODN for 24 h and then with cisplatin for 72 h were significantly increased. There were statistically significant difference in the percentage of apoptotic cells between hTR ASODN plus cisplatin and SODN plus cisplatin or cisplatin alone group. CONCLUSION: ASODN complementary to the template region of hTR can significantly suppress the telomerase activity and enhance cisplatin-induced apoptosis of K562 cells in vivo.
Key concepts: Cisplatin, Telomerase, Apoptosis, Agarose gel electrophoresis, Molecular biology, K562 cells, Biology, Annexin