Contributions
Abstract: PB1905
Type: Publication Only
Background
LW-213, a derivative of wogonin derived from traditional Chinese medicine plant Scutellaria baicalensis Georgi, has been shown anticancer activities on several breast cancer cell lines and xenograft models. Our previous results have reported the anti-leukemia effects of wogonin while the therapeutic effect of LW-213 in chronic myelogenous leukemia (CML) has been barely known.
Aims
To clarify whether LW-213 has better inhibitory effect on CML and its possible mechanism,
Methods
we explore the potency of this compound on K562, imatinib-resistant K562, and primary CML cells.
Results
These results showed that LW-213 inhibited proliferation of CML cells and induced cell cycle arrest in G2/M phase, leading to cell apoptosis. Meanwhile, LW-213 down-regulated cyclin dependent kinase 9 (CDK9) and inhibited phosphorylation of Stat3, down-regulating Mcl-1and cyclin B1. All results suggest that LW-213 triggered G2/M cell cycle arrest and apoptosis through the suppression of CDK9-related signaling pathways. In vivo, LW-213 prolonged survival of NOD/SCID mice inoculated with primary CML cells without any organ toxicity.
Conclusion
In conclusion, LW-213 might be a potential candidate compound on clinical treatment in imatinib-resistant CML patients.
Session topic: 7. Chronic myeloid leukemia – Biology & Translational Research
Keyword(s): Chronic myeloid leukemia
Abstract: PB1905
Type: Publication Only
Background
LW-213, a derivative of wogonin derived from traditional Chinese medicine plant Scutellaria baicalensis Georgi, has been shown anticancer activities on several breast cancer cell lines and xenograft models. Our previous results have reported the anti-leukemia effects of wogonin while the therapeutic effect of LW-213 in chronic myelogenous leukemia (CML) has been barely known.
Aims
To clarify whether LW-213 has better inhibitory effect on CML and its possible mechanism,
Methods
we explore the potency of this compound on K562, imatinib-resistant K562, and primary CML cells.
Results
These results showed that LW-213 inhibited proliferation of CML cells and induced cell cycle arrest in G2/M phase, leading to cell apoptosis. Meanwhile, LW-213 down-regulated cyclin dependent kinase 9 (CDK9) and inhibited phosphorylation of Stat3, down-regulating Mcl-1and cyclin B1. All results suggest that LW-213 triggered G2/M cell cycle arrest and apoptosis through the suppression of CDK9-related signaling pathways. In vivo, LW-213 prolonged survival of NOD/SCID mice inoculated with primary CML cells without any organ toxicity.
Conclusion
In conclusion, LW-213 might be a potential candidate compound on clinical treatment in imatinib-resistant CML patients.
Session topic: 7. Chronic myeloid leukemia – Biology & Translational Research
Keyword(s): Chronic myeloid leukemia