Mechanism of bortezomib in inducing apoptosis and improving chemosensitivity of Ishikawa cells / 南方医科大学学报
Journal of Southern Medical University
;
(12): 1301-1309, 2010.
Article
in Chinese
| WPRIM
| ID: wpr-336195
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of bortezomib on the apoptosis and drug sensitivity of endometrial cancer cell line Ishikawa cells.</p><p><b>METHODS</b>The IC50 of bortizomib, ADR, DDP and PTX in Ishikawa cells was determined using MTT method. After treatment with IC50 bortezomib for 6 and 12 h, the expressions of caspases-3, caspases-9 and bcl-2 genes were detected by RT-PCR, and the cell apoptotic rate and ROS level Ishikawa cells were evaluated by flow cytometry after treatment with half of the IC50 of the drugs for 24 h.</p><p><b>RESULTS</b>The IC50 of bortizomib, ADR, DDP, and PTX was 71.6 nmol/L, 0.572 micromol/L, 67.4 micromol/L and 719.5 nmol/L, respectively. Bortizomib significantly increased the mRNA expressions of caspases-3 and caspases-9 but decreased the expression of bcl-2. Compared with the treatment with agents alone, combined treatment of the cells significantly improved the cytotoxicity of the chemotherapeutic agents (P<0.05) and increased the ROS level and the apoptosis of the cells.</p><p><b>CONCLUSION</b>Bortizomib can inhibit the protein kinase to induce the apoptosis and enhance the chemosensitivity of Ishikawa cells.</p>
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pathology
/
Pharmacology
/
Protease Inhibitors
/
Pyrazines
/
Boronic Acids
/
Antineoplastic Combined Chemotherapy Protocols
/
Endometrial Neoplasms
/
Reactive Oxygen Species
/
Apoptosis
/
Proto-Oncogene Proteins c-bcl-2
Limits:
Female
/
Humans
Language:
Chinese
Journal:
Journal of Southern Medical University
Year:
2010
Type:
Article
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