Immunological effector cells enhance apoptosis induced by adriamycin in a multi-drug resistant human breast cancer cell line.
- Author:
Yong-jin SHI
1
;
Han-yun REN
;
Xi-nan CEN
;
Qiang ZHU
;
Ji-ren YU
Author Information
- Publication Type:Journal Article
- MeSH: ATP-Binding Cassette, Sub-Family B, Member 1; metabolism; Antibiotics, Antineoplastic; pharmacology; Apoptosis; drug effects; Breast Neoplasms; immunology; metabolism; pathology; Cell Line, Tumor; Down-Regulation; Doxorubicin; pharmacology; Drug Resistance, Multiple; Drug Resistance, Neoplasm; Female; Humans; Killer Cells, Lymphokine-Activated; immunology; Receptor, ErbB-2; metabolism
- From: Chinese Journal of Oncology 2006;28(3):188-191
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of immunologic effector cells to enhance apoptosis induced by adriamycin (ADR) in multi-drug resistant human breast cancer cell line MCF7/ADR.
METHODSThe immunologic effector cells were induced and expanded by IFN-gamma, McAb CD3, IL-1 and IL-2. The expression of P-glycoprotein (P-gp) and its relation to apoptosis in target cells were detected by TUNEL technique and immunohistochemical staining. Flow cytometry (FCM) was carried out to determine the expression level of human breast cancer related P185 antigen and the positive rate of Annexin V-FITC/PI expression. The subcellular distribution of ADR and Annexin V expression in the target cells were detected by fluorescence microscopy.
RESULTSThe immunologic effector cells down-regulated the expression of P185 and P-gp in MCF7/ADR cells. The accumulation and subcellular distribution of ADR in MCF7/ADR cells were increased after co-culture with the immunologic effector cells. After treatment with the immunologic effector cells in combination with ADR, apoptosis rate of the target cells was 10 times higher than that induced by ADR alone, and 13 times higher than that induced by the immunologic effector cells alone.
CONCLUSIONImmunologic effector cells can simultaneously down-regulate the expression of P185 and P-gp in MCF7/ADR cell line, and increase the apoptosis rate of MCF7/ADR cells in combination with ADR.
