THE EFFECTS OF JQ1 ON SUP-B15 CELL NOTCH1 PATHWAY AND ITS MECHANISMS
(Abstract release date: 05/21/15)
EHA Library. Liangming M. 06/12/15; 102588; PB1597
Disclosure(s): SHAN XI DA YI HOSPITALHEMATOLOGY
Ma Liangming
Contributions
Contributions
Abstract
Abstract: PB1597
Type: Publication Only
Background
Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL) has a poor prognosis. Advances of treatment due to the tyrosine kinase inhibitor imatinib have improved the cure rates.
Aims
The study was aimed to investigate the inducing effect of JQ1 on the apoptosis of Ph(+) human ALL Cell(SUP-B15),and whether the regulation of Notch1 pathway involved in the effect of JQ1 on SUP-B15 cells.
Methods
The SUP-B15 cell were treated with different concentrations of JQ1 for different time.The cell proliferation was analyzed with cytotoxicity test(MTT method).Cell cycle was detected by fluorescence microscopy and flow cytometry. The expression of Notch1 pathway was detected by real-time quantitative PCR by MSI2?Notch1?Hes1mRNA.
Results
The results indicated that JQ1 could significantly inhibite the viability of SUP-B15 cells treated with 0-4μmol/L in does-and time-dependent manner.JQ1 could induce S cycle arrest in does-dependent manner which was statistical different from the control at the same time (P<0.05).MIS2?Notch1?Hes1mRNA expression was down-regulated by JQ1 which was statistical different from the control(p<0.05)
Summary
It is concluded that JQ1 could potently inhibit the growth and proliferation of SUP-B15 cells and the Notch1 pathway might be one of the important apoptosis mechanisms in Ph(+) ALL cells induced by JQ1.
Keyword(s): Cell line, Oncogene, Ph+ ALL, Therapy
Type: Publication Only
Background
Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL) has a poor prognosis. Advances of treatment due to the tyrosine kinase inhibitor imatinib have improved the cure rates.
Aims
The study was aimed to investigate the inducing effect of JQ1 on the apoptosis of Ph(+) human ALL Cell(SUP-B15),and whether the regulation of Notch1 pathway involved in the effect of JQ1 on SUP-B15 cells.
Methods
The SUP-B15 cell were treated with different concentrations of JQ1 for different time.The cell proliferation was analyzed with cytotoxicity test(MTT method).Cell cycle was detected by fluorescence microscopy and flow cytometry. The expression of Notch1 pathway was detected by real-time quantitative PCR by MSI2?Notch1?Hes1mRNA.
Results
The results indicated that JQ1 could significantly inhibite the viability of SUP-B15 cells treated with 0-4μmol/L in does-and time-dependent manner.JQ1 could induce S cycle arrest in does-dependent manner which was statistical different from the control at the same time (P<0.05).MIS2?Notch1?Hes1mRNA expression was down-regulated by JQ1 which was statistical different from the control(p<0.05)
Summary
It is concluded that JQ1 could potently inhibit the growth and proliferation of SUP-B15 cells and the Notch1 pathway might be one of the important apoptosis mechanisms in Ph(+) ALL cells induced by JQ1.
Keyword(s): Cell line, Oncogene, Ph+ ALL, Therapy
Abstract: PB1597
Type: Publication Only
Background
Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL) has a poor prognosis. Advances of treatment due to the tyrosine kinase inhibitor imatinib have improved the cure rates.
Aims
The study was aimed to investigate the inducing effect of JQ1 on the apoptosis of Ph(+) human ALL Cell(SUP-B15),and whether the regulation of Notch1 pathway involved in the effect of JQ1 on SUP-B15 cells.
Methods
The SUP-B15 cell were treated with different concentrations of JQ1 for different time.The cell proliferation was analyzed with cytotoxicity test(MTT method).Cell cycle was detected by fluorescence microscopy and flow cytometry. The expression of Notch1 pathway was detected by real-time quantitative PCR by MSI2?Notch1?Hes1mRNA.
Results
The results indicated that JQ1 could significantly inhibite the viability of SUP-B15 cells treated with 0-4μmol/L in does-and time-dependent manner.JQ1 could induce S cycle arrest in does-dependent manner which was statistical different from the control at the same time (P<0.05).MIS2?Notch1?Hes1mRNA expression was down-regulated by JQ1 which was statistical different from the control(p<0.05)
Summary
It is concluded that JQ1 could potently inhibit the growth and proliferation of SUP-B15 cells and the Notch1 pathway might be one of the important apoptosis mechanisms in Ph(+) ALL cells induced by JQ1.
Keyword(s): Cell line, Oncogene, Ph+ ALL, Therapy
Type: Publication Only
Background
Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL) has a poor prognosis. Advances of treatment due to the tyrosine kinase inhibitor imatinib have improved the cure rates.
Aims
The study was aimed to investigate the inducing effect of JQ1 on the apoptosis of Ph(+) human ALL Cell(SUP-B15),and whether the regulation of Notch1 pathway involved in the effect of JQ1 on SUP-B15 cells.
Methods
The SUP-B15 cell were treated with different concentrations of JQ1 for different time.The cell proliferation was analyzed with cytotoxicity test(MTT method).Cell cycle was detected by fluorescence microscopy and flow cytometry. The expression of Notch1 pathway was detected by real-time quantitative PCR by MSI2?Notch1?Hes1mRNA.
Results
The results indicated that JQ1 could significantly inhibite the viability of SUP-B15 cells treated with 0-4μmol/L in does-and time-dependent manner.JQ1 could induce S cycle arrest in does-dependent manner which was statistical different from the control at the same time (P<0.05).MIS2?Notch1?Hes1mRNA expression was down-regulated by JQ1 which was statistical different from the control(p<0.05)
Summary
It is concluded that JQ1 could potently inhibit the growth and proliferation of SUP-B15 cells and the Notch1 pathway might be one of the important apoptosis mechanisms in Ph(+) ALL cells induced by JQ1.
Keyword(s): Cell line, Oncogene, Ph+ ALL, Therapy
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