Drug Resistance, Neoplasm ; Humans ; Multiple Myeloma

The study was aimed to investigate the effect of quercetin, flavonoid molecules on reversing leukemia multidrug resistance and its mechanism. K562/A cells were cultured in vitro with different concentrations of quercetin. Cell growth inhibition and adriamycin (ADR) sensitivity were detected by MTT method. Intracellular ADR concentration was determined by flow cytometry. Cell apoptosis was assayed by Annexin V/PI staining method. The expressions of drug transporter and apoptosis related genes were measured by real-time PCR array. The results indicated that quercetin inhibited the proliferation of K562 and K562/A in 5-160 µmol/L and with dose-dependent manner. Quercetin increased the sensitivity of K562/A cells to ADR in a low toxicity concentration. Flow cytometry showed that the quercetin increased the accumulation of ADR in K562/A cells when cells were co-cultured with 5 µmol/L ADR for 2 hours. Quercetin could induce the apoptosis of K562 and K562/A cells with dose dependent manner. Furthermore, some drug transport related genes such as ATP-binding cassette (ABC) and solute carrier (SLC) and some apoptosis-related genes such as BCL-2, tumor necrosis factor (TNF), tumor necrosis factor receptor (TNFR) families were down-regulated by quercetin. It is concluded that quercetin reverses MDR of leukemic cells by multiple mechanisms and the reversing effect is positively related to drug concentration.
Drug Resistance, Multiple ; drug effects ; Drug Resistance, Neoplasm ; drug effects ; Humans ; K562 Cells ; Quercetin ; pharmacology

Major progress in the management of osteosarcoma has been made due to advances in diagnostic imaging, operative technique, and chemotherapy, resulting in an improved survival. However, 20~30% of patients with osteosarcoma still develop distant metastases despite combined modality treatment. Currently various experimental efforts are being proposed to the future new strategy include drug resistance, suppression of metastasis mechanism, and targeted therapy to convert the incurable rate of 20~30% upto complete cure rate.
Diagnostic Imaging ; Drug Resistance ; Drug Therapy ; Humans ; Neoplasm Metastasis ; Osteosarcoma*

Drug Resistance, Neoplasm ; Humans ; Stomach Neoplasms ; drug therapy

Drug therapy is one of the efficient methods for prostate cancer treatment. However, drug resistance greatly hindered the treatment of prostate cancer patients. Herein, the mechanisms of drug resistance in prostate cancer have been exhaustively reviewed, and that can provide an alternative strategy and new targets for anti-prostate cancer therapy.
Drug Resistance, Neoplasm ; Humans ; Male ; Prostatic Neoplasms ; drug therapy

Gastric cancer is one of the most common human malignancies and the third cause of death from cancer in China and worldwide. Chemotherapy is still one of the major treatment options for advanced gastric cancer. However,the efficacy of chemotherapy for gastric cancer remains poor due to its insensitivity and the development of multidrug resistance (MDR). While many molecules and mechanisms have been found to be associated with the development of gastric cancer MDR,the specific mechanisms remains unclear. In our current article,we reviews the identification of MDR-related molecules and mechanisms,with an attempt to a better understand the specific mechanisms of gastric cancer MDR and thus provide new insights into the fight against gastric cancer MDR.
Drug Resistance, Multiple ; Drug Resistance, Neoplasm ; Humans ; Stomach Neoplasms ; drug therapy

Non-Hodgkin's lymphoma (NHL) is a malignant tumor originated in lymphatic hematopoietic tissue. At present, chemotherapy is the main treatment method of NHL, but the chemoresistance is still an important reason for NHL treatment failure. The mechanism of NHL multidrug resistance (MDR) is complex, involving a variety of singnal pathways, in which mutation in the genetic level of the key genes can result in tumor cell resistance phenomenon. MicroRNA are small non-coding RNA that can be widely detected in plants,animal species and viruses. They regulate protein expression by repressing translation mRNA target at the post-transcriptional level, participating in the differentiation and development of tumor cells, as well as the occurrence and development of tumor, the change of the expression level microRNA plays an important role in the genesis and chemoresistance mechanism of NHL. Therefore, the intervening factitiously the expression level of microRNA in NHL through manufacturing antisense oligonucleotide (AMO) or using substitution of microRNA, changing the expression level of their target protein, and combining with the therapy of NHL, there will be an guiding significance in reversing the drug and radiation resistance of NHL, thus improving its poor prognosis. This article reviews the microRNAs closely related with drug and radiation resistance of NHL, and their potential targets. Furthermore, the specific role of these microRNAs in the genesis and chemoresistance mechanism of NHL are deeply elaborated.
Animals ; Drug Resistance, Multiple ; Drug Resistance, Neoplasm ; Lymphoma, Non-Hodgkin ; drug therapy ; genetics ; MicroRNAs ; genetics

OBJECTIVETo study the drug resistance changes in Tca8113 cell lines by exposing to carboplatin.

METHODSThe concentration of carboplatin added to Tca8113 cells was increased gradually and continually, which was to induce the carhoplatin-resistance in Tca8113 cells. The sensibility to drugs of the cells was analyzed by MTT method. Immunocytochemistry and RT-PCR were utilized to examine the expression of multidrug resistance proteins and genes.

RESULTSAfter exposing to carboplatin, the Tca8113/CBP cells had higher drug-resistance to CBP, MTX, PYM, VCR and higher expression of MRP, GST-pi than Tca8113 cells.

CONCLUSIONMultidrug resistance of Tca8113/CBP is associated with over expression of MRP, GST-pi and MDR. Tca8113/CBP can provide an ideal model for multidrug resistance research.

Multidrug resistance (MDR), defined as the resistance of cancer cells to compounds with diverse structures and mechanisms of actions, significantly limits the efficacy of antitumor drugs. A major mechanism that mediates MDR in cancer is the overexpression of adenosine triphosphate (ATP)-binding cassette transporters. These transporters bind to their respective substrates and catalyze their efflux from cancer cells, thereby lowering the intracellular concentrations of the substrates and thus attenuating or even abolishing their efficacy. In addition, cancer cells can become resistant to drugs via mechanisms that attenuate apoptosis and cell cycle arrest such as alterations in the p53, check point kinase, nuclear factor kappa B, and the p38 mitogen-activated protein kinase pathway. In this review, we discuss the mechanisms by which β-elemene, a compound extracted from Rhizoma zedoariae that has clinical antitumor efficacy, overcomes drug resistance in cancer.
Antineoplastic Agents ; Apoptosis ; Drug Resistance, Multiple ; Drug Resistance, Neoplasm ; Humans ; Neoplasms ; Pinellia ; Sesquiterpenes

Drug Resistance, Multiple ; radiation effects ; Drug Resistance, Neoplasm ; radiation effects ; Hep G2 Cells ; Humans ; X-Rays