Autophagy is a biological process in which cells maintain homeostasis through degradation of cytoplasmic macromolecules and damaged organelles by membrane vesicle structure .Autophagy plays a critical role in maintai-ning survival of intestinal epithelial cells during intestinal mucosal barrier dysfunction .A negative regulator of auto-phagy may lead to intestinal inflammation and tumorigenesis .

Multidrug resistance (MDR) limits the clinical application and efficacy of chemotherapy drugs. Thus, MDR is the big-gest obstacle to the success of chemotherapy. Complex and diverse MDR mechanisms exist, including the following:adenosine triphos-phate-binding cassette membrane transport protein family, anti-apoptotic or enhanced DNA repair, mutations in drug targets or metabol-ic enzymes, microRNA, and cancer stem cells. Autophagy can degrade organelles and proteins that have been damaged in the cyto-plasm through the formation of autolysosome and recycle metabolites. Maintaining intracellular homeostasis and a balanced internal en-vironment is highly significant. Recent studies found that autophagy is closely related to the pathophysiology of MDR. The interaction between autophagy and MDR and the possible molecular mechanisms underlying these phenomena are reviewed. This paper elucidates the occurrence of MDR in relation to autophagy in order to provide new information on chemotherapy MDR.

Objective To study the effect of repeated rectal exposure of low -dose simian immunodeficiency virus on the systemic cellular immunity in monkeys .Methods Eight 3-to 4-year old rhesus macaques ( Macaca mulatta) (male:female 1:1) were used in this study.The monkeys were inoculated with 10 TCID50 SIVmac239 virus through rectum twice a week for consecutive 6 weeks to establish a multiple rectal exposure model of SIVmac 239 virus infection.Then, plasma viral load, CD4+ T cell count, T cell subsets and IFN-γsecretion of the experiment monkeys were determined . Results Low-dose SIVmac239 virus induced some changes in the immune system through the rectal mucosa , but didn’t induce typical infection.Repeated rectal mucosal low-dose virus exposure can activate the cellular immune system . Conclusions This study defines the effect of repeated low -dose simian immunodeficiency virus exposure on the systemic cellular immunity, and provided basic information for HIV-1 vaccine research.

Objective To investigate the effect and mechanism of osteopontin(OPN)in hepatoma cell migration through galectin-3 binding protein(LGALS3BP).Methods Human hepatoma cell lines SMMC-7721,SMMC-P(stably transfected with empty eukaryotic expression vectors),and SMMC-OPN(stably transfected with the OPN gene)were cultured.mRNA expression levels of OPN and LGALS3BP were measured by RT-qPCR.Western blot assays were used to analyze the relative protein expression of OPN and LGALS3BP and PI3K/AKT pathway.Wound healing assays were performed to explore the cell migration ability.After transfection with LGALS3BP-targeting small interfering RNA(si-LGALS3BP)or negative control small RNA(si-NC)into SMMC-OPN cells,cell migration and relative expression of PI3K/AKT pathway-related proteins were assessed.Results Compared with SMMC-7721 and SMMC-P,the migratory ability of SMMC-OPN cells was significantly reinforced,and expression of LGALS3BP was obviously upregulated at both mRNA and protein levels.Moreover,relative expression of p-PI3K/PI3K and p-AKT/AKT proteins was significantly increased.Wound healing assays showed that the si-LGALS3BP obviously suppressed the migratory ability of SMMC-OPN cells.Furthermore,relative expression of p-PI3K/PI3K and p-AKT/AKT proteins in SMMC-OPN cells was significantly decreased after transfection of si-LGALS3BP.Conclusions OPN activates the PI3K/AKT pathway by upregulating LGALS3BP expression to promote hepatoma cell migration.