Curcumin Increases the Chemosensitivity of Multiple Myeloma to Bortezomib by Inhibiting the Notch1 Signaling Pathway.
10.19746/j.cnki.issn.1009-2137.2019.02.025
- Author:
Xue-Ping GE
1
;
Ya-Ting HONG
1
;
Ya-Li LI
1
;
Bing-Zong LI
2
Author Information
1. Department of Hematology, The Second Affiliated Hospital of Soochow University, Suzhou 215006, Jiangsu Province, China.
2. Department of Hematology, The Second Affiliated Hospital of Soochow University, Suzhou 215006, Jiangsu Province, China,E-mail: lbzwz0907@hotmail.com.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Bortezomib;
Cell Line, Tumor;
Cell Proliferation;
Curcumin;
Humans;
Multiple Myeloma;
Receptor, Notch1;
Signal Transduction
- From:
Journal of Experimental Hematology
2019;27(2):464-471
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To evaluated the effect of curcumin on the bortezomib-resistant myeloma cells and the expression of Notch1 signaling pathway, in order to further explore its potential mechanism.
METHODS:Curcumin, bortezomib, and curcumin combined bortezomib were added into RPMI 8266, U266, 5 nmol/L bortezomib-resistant RPMI 8266 (RPMI 8226-V5R), 5 nmol/L bortezomib-resistant U 266 (U266-V5R) and CD138+ plasma cells respectively. The cell proliferation was measured by MTT assay. the apoptotic rate was determined by flow cytometry, and the Western blot was used to detect the expression of apoptosis-related proteins. Then, the expression of Notch1 in cells was inhibited by notch1 inhibitor DAPT and RNA interference, the above-motioned experiments should be repeated.
RESULTS:Compared with single drug-treated groups, the treatment with 2 drugs could further inhibit cell proliferation, induce apoptosis and enhance the inhibition effect on notch1 signaling pathway (P<0.05), while the inhibiting Notch1 signaling pathway could reduce cell proliferation and increase the expression of cleaved caspase-3.
CONCLUSION:Curcumin can increase chemosensitivity of myeloma cells to bortezomib, this effect may be related to the inhibition of Notch1.
