The glucose metabolism pathways including glycolysis and oxidative phosphorylation in vivo.The metabolism of tumor cells depends on glycolysis,which enhances the adaptability of tumor cells to the microenvironment and promotes the proliferation of tumor cells,which is called Warburg effect.Arsenic is one of the chemical pollutants,which is widely distributed in natural environment.International agency for research on cancer (IARC) has made it clear that arsenic and its compounds are carcinogens.However,the mechanism of carcinogenesis induced by arsenic still remains obscure.Recently,researchers have found that Warburg effect plays an important role in the process of arsenic carcinogenesis.In this paper,we have reviewed the definition and function of glycolysis,its relationship with inflammation and tumorigenesis,and the role of Warburg effect in arsenic carcinogenesis.

Objective To investigate the role of exosomal microRNA(miR)-191 derived from NaAsO2-transformed cells in proliferation of human liver L-02 cells.Methods The normal wild-type L-02 cells (recipient L-02 cells)were treated with media or exosome derived from 2 μmol/L NaAsO2-transformed L-02 cells.Anti-miR-191 and anti-miR-NC were transfected into NaAsO2-transformed L-02 (T-L-02) cells by lipofectamineTM 2000,respectively,while untreated group was set as control.The expression of miR-191 was detected by qRT-PCR.Cell proliferation was evaluated by CCK-8 assay.Results The proliferation [(207 ± 24)％ vs (105 ± 21)％,t =5.462,P ＜ 0.01] and the expression of miR-191 [(206 ± 25)％ vs (105 ± 20)％,t =4.116,P ＜ 0.05] of recipient L-02 cells were significantly increased in the transformed L-02 cells media (T-CM) treated group compared with in the normal L-02 cells media (CM) group.Several concentrations of exosomes derived from CM did not change the proliferation and miR-191 expression of recipient L-02 cells (F =2.213,2.213,all P ＞ 0.05).Several concentrations of exosomes derived from T-CM increased the proliferation and miR-191 expression of recipient L-02 cells in a dose-response manner (F =10.910,4.553,P ＜ 0.01 or ＜ 0.05).The proliferation [(160 ± 32)％ vs (102 ± 8)％,(203 ± 7)％ vs (111 ± 5)％,t =2.999,18.750,P ＜ 0.05 or ＜ 0.01] of recipient L-02 cells treated with 20 or 50 mg/L exosomes derived from T-CM was higher than that treated with the same concentration of exosomes derived from CM.The expression of miR-191 [(166 ± 13)％ vs (113 ±9)％,(211 ± 55)％ vs (102 ± 8)％,(206 ± 31)％ vs (105 ± 6)％,t =5.611,3.357,5.509,P ＜ 0.05 or ＜ 0.01] of recipient L-02 cells treated with 10,20 or 50 mg/L exosomes derived from T-CM was higher than that treated with the same concentration of exosomes derived from CM.The miR-191 levels of T-L-02 cells [(39 ± 10)％ vs (100 ± 0)％ or (106 ±17)％,all P ＜ 0.01] or exosomes [(30 ± 19)％ vs (100 ± 0)％ or (104 ± 17)％,all P ＜ 0.01] in the anti-miR-191 treated group were significantly lower than that in the untreated group or anti-miR-NC treated group.The exosomes derived from untreated group promoted the proliferation [(395 ± 31)％ vs (100 ± 0)％,t =16.290,P ＜ 0.01] and miR-191 expression [(208 ± 47)％ vs (100 ± 0)％,t =4.015,P ＜ 0.05] of recipient L-02 cells.The proliferation [(157 ± 19)％ vs (395 ± 31)％ or (411 ± 55)％,P ＜ 0.05] and miR-191 expression of [(103 ± 44)％ vs (208 ± 47)％ or (197 ± 37)％,P＜ 0.05 or ＜ 0.01] of recipient L-02 cells treated with exosomes derived from anti-miR-191 treated group were lower than those treated with exosomes derived from untreated group or anti-miR-NC treated group.Conclusion The exosomal miR-191 secreted by NaAsO2-transformed L-02 cells promotes proliferation of normal human L-02 cells.

OBJECTIVE: To determine the screening of the expression of membrane proteins in androgen-dependent prostate cancer (ADPC) and androgen-independent prostate cancer (AIPC) and to explore the mechanism of membrane proteins in these two cancers. METHODS: Serum samples were collected from 3 patients with ADPC and another 3 patients with AIPC. The serum was incubated with ADPC cell line LNCaP and/or AIPC cell line PC-3 and detected by immunoprecipitation and Western blot. Differentially expressed proteins between ADPC and AIPC identified by mass spectrometry were compared and their expression level and location were analyzed by immunofluorescence. RESULTS: Altogether 11 membrane proteins were identifited, such as the Neural-Cadherin precursor, ER60 precursor, Claudin-4, and so on. Immunofluorescence revealed that the expression level of Claudin-4 in PC-3 cells was higher than in LNCaP cells. CONCLUSION We can use the screening method to study membrane proteins in prostate cancer. Claudin-4 may play an important role in the pathogenesis and the development of AIPC.
Aged ; Androgens ; genetics ; metabolism ; Cell Line, Tumor ; Claudin-4 ; genetics ; metabolism ; Gene Expression Profiling ; Humans ; Male ; Membrane Glycoproteins ; genetics ; metabolism ; Prostatic Neoplasms ; genetics ; metabolism ; pathology ; Protein Disulfide-Isomerases ; genetics ; metabolism