Experimental study of sensitivity to chemotherapeutic agents for human endometrial carcinoma cell line.
- Author:
Xiu-gui SHENG
1
;
Ling TANG
;
Da-peng LI
;
Hui-qin LI
;
Xian-rang SONG
;
Chun-hua LU
;
Xing-wu WANG
;
Qing-shui LI
Author Information
- Publication Type:Journal Article
- MeSH: ATP-Binding Cassette, Sub-Family B, Member 1; metabolism; Antineoplastic Agents; administration & dosage; pharmacology; Apoptosis; drug effects; Carboplatin; administration & dosage; pharmacology; Cell Cycle; drug effects; Cell Line, Tumor; Dose-Response Relationship, Drug; Doxorubicin; administration & dosage; pharmacology; Drug Resistance, Multiple; Drug Resistance, Neoplasm; Endometrial Neoplasms; metabolism; pathology; Epirubicin; administration & dosage; pharmacology; Female; Fluorouracil; administration & dosage; pharmacology; Humans; Organoplatinum Compounds; administration & dosage; pharmacology
- From: Chinese Journal of Oncology 2004;26(7):409-412
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo screen the sensitive chemotherapeutic agents to human endometrial carcinoma cell line-1 (HECCL-1) and study its mechanism.
METHODSMTT method was used to examine the relative inhibition ratios (RIRs) of various concentrations of 18 chemotherapeutic agents to HECCL-1. Cell cycle, apoptosis and expression of MDR1 protein were detected by FCM.
RESULTSNine of the chemotherapeutic agents studied obviously inhibited the proliferative activity of HECCL-1 in a dose-dependent manner. The order of sensitivity was as follows: adriamycin (ADM), oxaliplatin (L-OHP), carboplatin (CBP), cisplatin (DDP), taxol (TAL), epirubicin (EPI), mitoxantrone (MIT), dactomycin (ACTD) and 5-fluorouracil (5-Fu). FCM showed these agents could significantly reduce the proportion of cells in G0-G1 phase, and increase the proportion of cells in S and G2-M phase (P < 0.05). Cell apoptosis was observed in 11 chemotherapeutic agents at their peak concentration. MDR expression was induced after using EPI, 5-Fu, hydroxycamptothecin (HCPT) and MIT.
CONCLUSIONHECCL-1 is sensitive to a number of the chemotherapeutic agents studied. Induced apoptosis may be the major mechanism of drug sensitivity, and acquired drug-resistance may be the critical reason against continued administration.
