Multidrug resistance (MDR) refers to the emergence of resistance of tumor cells to one antitumor drug while at the same time they are resistant to a variety of other antitumor drugs with different structures and different target sites of action. With the wide application of tumor chemotherapeutic drugs, the problem of tumor drug resistance has become more and more prominent, and has become one of the main obstacles to the effective treatment of tumors. At present, the study of tumor drug resistance mechanism mainly starts from the products of MDR gene expression to explore the resistance mechanism caused by such products. The main ones are P-glycoprotein (P-gP), intracellular reduced glutathione (GSH) and glutathione transferase (GST), DNA topoisomerase Ⅰ, Ⅱ (TOPO Ⅰ, Ⅱ), multidrug resistance-related protein (MRP) and lung resistance protein (LRP). Yan Speed, Department of Surgical Oncology, Affiliated Hospital of Qinghai University P-glycoprotein (P-gP) P-gP is a transmembrane glycoprotein, produced by the MDR1 gene encoding, acts as an efflux pump, which pumps antitumor drugs out of the cell against the concentration of antitumor drugs to the outside of the cell, decreasing the concentration of intracellular drugs and leading to tumor Drug resistance. This glycoprotein is composed of two identical monomers of 1281 amino acids, each with six transmembrane regions and one adenosine triphosphate (ATP) binding site. The transmembrane region facilitates drug transport as a membrane channel, while the ATP binding site is associated with energy supply. Numerous studies have proved that high expression of P-gP is accompanied by poor prognosis of tumor patients, such as low remission rate, high recurrence rate, poor efficacy of chemotherapy and short survival period. Intracellular reduced glutathione (GSH) and glutathione transferase (GST) GSH overexpression can bind to the oxidized substances of chemotherapeutic drugs, thus preventing chemotherapeutic drugs from attacking tumor cells, and thus generating drug resistance.There are three types of GST: α (alkaline), π (acidic), and μ (neutral), which catalyzes the binding of GSH to chemotherapeutic drugs.The intensity of the expression of GSH and GST is related to the average survival period. The intensity of GSH and GST expression is related to the average survival period, and the higher the intensity of expression, the shorter the survival period.GSH and GST can also protect cells against the damage caused by radiotherapy, thus producing tolerance to radiotherapy. DNA topoisomerases (TOPO I and II) DNA topoisomerases are basic nuclear enzymes that catalyze local conformational changes in the superhelical structure of DNA. Chemotherapeutic agents cross-link with DNA to form covalent complexes, which can split the complexes and cause DNA breaks, leading to tumor cell death.DNA topoisomerase is also an important target for many chemotherapeutic agents, which leads to a decrease in the enzyme’s activity or activity, resulting in fewer complexes that can be split, less DNA damage to the tumor cells, and reparative power, so that the tumor cells do not die due to DNA breaks, thus creating drug resistance. death, resulting in drug resistance.Kellaer et al. detected a 20-fold higher level of TOPO II in sensitive cells than in drug-resistant tumor cells. Multidrug resistance-associated protein (MRP) MRP is also a transmembrane glycoprotein, and it is known that increased MRP1 is one of the major causes of MDR, playing an important role in the transmembrane transport of a range of molecules in prokaryotes and eukaryotes. It is also an ATP-dependent pump that pumps negatively charged drug molecules out of the cell against concentration, reducing intracellular drug concentrations and leading to the development of tumor resistance. It can also reduce the concentration of the drug when it reaches the target site at the site of action by changing the pH of the cell plasma and organelles, generating tumor resistance and directly participating in tumor metastasis.The expression of MRP is associated with the changes in the S-phase of the cell cycle. Foreign researchers believe that MRP overexpression occurs earlier and P-gP expression later in the mechanism of acquired MDR generation.Filipits et al. detected MRP expression in paraffin tissue sections of 30 cases of colorectal cancer and proved that strong positive expression of MRP was not related to tumor stage, differentiation degree and prognosis. Domestic researchers also detected MRP and LRP expression in 52 cases of human rectal cancer tissues. The study showed that there was no significant correlation between the positive rate of MRP or LRP expression and tumor stage and degree of differentiation, and the postoperative survival of those with positive MRP expression was significantly lower than that of those with negative expression.MRP may be one of the indicators for determining the prognosis of human rectal cancer, and it is of guiding significance for the implementation of comprehensive treatment for rectal cancer patients. Lung Resistance Protein (LRP) The mechanism by which LRP causes MDR is as follows: LRP prevents the transport of drugs that use the nucleus as an effector into the cytoplasm; transports drugs that enter the cytoplasm into transport vesicles, which segregate them from drug action, and excretes them from the body by cytosolization, thus generating resistance.LRP is not exclusively present in lung tumors, but is widely distributed in normal tissues, with tissue-specificity, and is found in tissues such as rectal, leukemia, and ovarian cancers. It is widely distributed in normal tissues and has tissue specificity, with high expression in rectal cancer, leukemia, ovarian cancer and other tissues, especially in epithelial tissues with secretion and excretion functions. Studies have shown that there is no significant correlation between the expression of LRP in rectal cancer tissues and the prognosis.