Apoptosis-regulating factors and drug resistance.docVIP

 PAGE \* MERGEFORMAT 32 Apoptosis-regulating factors and drug resistance Tumor cells to chemotherapeutic drug resistance is an important reason for failure of clinical chemotherapy. This paper reviews the apoptosis regulator p53, bcl-2, bax and other drug resistance mechanisms of tumor cells, p53 protein, such as the impact of the P-glycoprotein and multidrug resistance-associated protein regulates the expression of the role and introduce some of multidrug resistance The new research. Radiotherapy and chemotherapy on tumor cells significantly in vitro. However, a major obstacle to successful treatment of tumor cells to the treatment of non-response, and the emergence of resistance cell populations, leading to cancer recurrence or invasive progress. Therefore, learn the basis of cellular resistance to chemotherapeutic drugs in many experimental studies of hot spots. In general, the focus of the study is to explain how the treatment of factors to achieve intracellular target sites, and check the interaction between drugs and the molecular basis of target sites, such as the high levels of MDRI gene expression in a variety of drugs can limit the concentration of cells, and caused by multidrug resistance (MDR). In recent years, to explore and understand the mechanism of apoptosis of tumor cells to acquire or lose their cytotoxic mechanism of tolerance to a new understanding. An apoptosis-regulating factors on the regulation of drug resistance Many drugs can induce apoptosis, including anti-metabolism drugs, deoxy-nucleotide synthesis inhibitors, DNA topoisomerase inhibitors, alkylating agent, and interfering with microtubule drugs, etc. [1]. Chemotherapy drug-induced apoptosis in the process is not very clear of drugs may be interrupted due to the normal cell cycle [2]. Apoptosis is a kind that can be activated or inhibited may be the adjustment process, so there may in some cases, a new interpretation of drug r