Multidrug resistance (MDR) is the major obstacle to successful chemotherapy of human malignancies and strategies for overcoming MDR phenomena are still unavailable to clinical use. Previous results showed that ultrasound (US) exposure could make MDR cancer cells become more sensitive to anticancer drugs, and the physical parameters of US exposure could adjust the uptake and retention of rhodamine 123 in MDR cells. In this study, we investigated the mechanisms of therapeutic ultrasound as a physical approach to overcoming MDR in a multidrug resistant human hepatocarcinoma cell line (HepG2/ADM).
View Article and Find Full Text PDFPrevious studies have shown that ultrasound (US) could enhance cellular uptake and cytotoxicity of chemotherapeutic agents in drug-resistant cancer cells. The goal of this study was to investigate the optimization of physical parameters of US exposure for in vitro reversal of multidrug resistance (MDR) in human hepatocarcinoma cell line (HepG2). Using a constant total energy density (3.
View Article and Find Full Text PDFMultidrug resistance (MDR) is one of the major obstacles to successful chemotherapy of human malignancies. Although many strategies have been explored to overcome MDR, none of them have been proven to be clinically useful until now. The aim of this study was to investigate whether a novel therapeutic ultrasound (US) approach would have useful effects on the reversal of MDR in cancer cells.
View Article and Find Full Text PDFWorld J Gastroenterol
November 2006
Aim: To establish a multidrug resistant (MDR) cell sub-line from the human hepatocarcinoma cell line (HepG2) in nude mice.
Methods: HepG2 cell cultures were incubated with increasing concentrations of adriamycin (ADM) to develop an ADM-resistant cell subline (HepG2/ADM) with cross-resistance to other chemotherapeutic agents. Twenty male athymic BALB/c-nu/nu mice were randomized into HepG2/nude and HepG2/ADM/nude groups (10 in each group).
Background & Objective: Multidrug resistance (MDR) phenotype is the obstacle of chemotherapy in tumors and inspired research interesting. This study was to establish multidrug resistance (MDR) models induced with adriamycin in vivo of subcutaneous or in situ hepatic transplanted human liver cancer in nude mice (BALB/C nu/nu), and explore the biological characteristics and mechanism of multidrug resistance, which can provide an ideal animal model for the basic,and clinical study of MDR.
Methods: After successful performing either subcutaneous or hepatic transplantation in nude mice with liver cancer cell line HepG2, adriamycin (ADM) was injected into abdominal cavity to induce multidrug resistance.
Background & Objective: Multidrug resistance (MDR) is considered to be the major obstacle for chemotherapy. In order to reverse tumor MDR in vitro, we designed this study to establish human multidrug-resistant hepatocellular carcinoma cell line (HepG2/Adm) and to investigate its biological characteristics.
Methods: An adriamycin-resistant human hepatocellular carcinoma cell subline (HepG2/Adm) was established in vitro using gradually increased concentration of adriamycin (ADM) in culture.
Objective: To establish human hepatocellular carcinoma multidrug-resistance cell line (HepG2/ADM) and to determine the effect of low-frequency pulse ultrasound (US) on MDR cells and investigate its mechanism.
Methods: Using gradual increase of adriamycin (ADM) concentrations in culture, an adriamycin-resistant human hepatocellular carcinoma cell sub line (HepG2/ADM) was established in vitro. HepG2/ADM cells were cultured in vitro and randomly divided into 4 groups: the control group (HepG2/ADM only), the group ADM by 1.
Background & Objective: The effects of ultrasound have been shown on increasing cell membrane permeability and thereby might promote cellular uptake of cytotoxic drugs and enhance chemotoxicity. The aim of this study was to examine the reversal effects of high intensity focused ultrasound (HIFU) and co-administration with Adriamycin (ADM) on multidrug resistance (MDR) in HepG2/Adm cells, and to investigate its mechanism.
Methods: HepG2 cells and HepG2/Adm cells were divided into 4 groups: HepG2 (control group),HepG2 (treated with HIFU 5s),HepG2/Adm (non HIFU), and HepG2/Adm (treated with HIFU 5s).