OBJECTIVE: To assess the effect of celecoxib in combination with adriamycin(ADM) on cell proliferation and apoptosis. METHODS: Cell lines were treated with celecoxib,and cell proliferation was examined by the method of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) at different time. The cellular apoptotic rate was analyzed by flow cytometry. RT-PCR was applied to distinguish the level of caspase-9 mRNA expression. Immunohistochemistry was used to detect the caspase-9 protein expression in Raji cells. RESULTS: Celecoxib inhibited the proliferation and increased the apoptosis of Raji cell lines in a dose-dependent and time-dependent manner within 20-100 μmol/L. Compared with the celecoxib alone, the proliferation of Raji cell lines incubated with celecoxib and adriamycin was decreased. Caspase-9 mRNA and protein expression in Raji cells were significantly enhanced after the treatment of celecoxib (P<0.05). CONCLUSION Celecoxib can inhibit the proliferation of Raji cells in a dose-dependent and time-dependent manner. Celecoxib may lead to the apoptosis of Raji cells by up-regulating activities of caspase-9. Adriamycin could intensify the effect.
Apoptosis ; drug effects ; Burkitt Lymphoma ; pathology ; Caspase 9 ; genetics ; metabolism ; Celecoxib ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Dose-Response Relationship, Drug ; Doxorubicin ; pharmacology ; Drug Synergism ; Humans ; Pyrazoles ; pharmacology ; RNA, Messenger ; genetics ; metabolism ; Sulfonamides ; pharmacology

Objective To identify the rate of hepatitis B virus (HBV) reactivation and potential risk factors in hepatitis B surface antigen negative/hepatitis B core antibody positive patients with lung cancer receiving adjuvant chemotherapy without concomitant antiviral prophylaxis.Methods The records of 3280 patients with lung cancer who received adjuvant chemotherapy were retrospectively reviewed from January 2003 to December 2011.Among these patients,367 hepatitis B surface antigen negative/hepatitis B core antibody positive patients were analyzed for the HBV reactivation in this study.The HBV serology marker and biochemical tests of the 367 patients were performed.The data were analyzed by chi square test.Results Among 367 hepatitis B surface antigen negative/hepatitis B core antibody positive patients with lung cancer,14 patients suffered HBV reactivation.Univariate analysis showed that age≥70 years(x2 =13.003,P=0.019),abnormal liver computed tomography findings (x2 =11.225,P =0.026) and the amount of corticost eroids≥ 150 mg(x2 =7.008,P =0.033)were associated with HBV reactivation.However,gender and adjuvant chemotherapy regimens were not related with HBV reactivation.Conclusion HBV reactivation occurs in a proportion of hepatitis B surface antigen negative/hepatitis B core antibody positive patients with lung cancer during adjuvant chemotherapy.

OBJECTIVE: To determine the effect of arsenic trioxide combined with adriamycin(ADM) on the proliferation and apoptosis of human lymphoma cells. METHODS: Raji cells were divided into an experimental group and a control group, and the experimental group was further divided into 1 micromol/L As(2)O(3) group,2 micromol/L As(2)O(3) group, ADM group,1 micromol/L As(2)O(3) and ADM group,2 micromol/L As(2)O(3) and ADM group. Human lymphoma cells Raji were treated with As(2)O(3) combined with ADM. Wright-Giemsa dying assay was used to observe the apoptosis morphology of lymphoma cells. The proliferation of the cells treated with As(2)O(3) and adriamycin was detected by the method of 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide(MTT). Flow cytometry(FCM) was used to detect the apoptosis rate of lymphoma and the fluorescene density in the lymphocytes. Effect of arsenic trioxide and adriamycin on the mutant p53 expression in Raji cells was detected by semi-quantitive RT-PCR. RESULTS: Evident apoptotic morphological changes of Raji cells were observed 24 hours after treatment with As(2)O(3) or ADM. Compared with As(2)O(3) or ADM alone, As(2)O(3) combined with ADM could increase the inhibition ratio significantly (P<0.05), and the inhibition rate was related to the concentration and action time of As(2)O(3) (P<0.05). Compared with As(2)O(3) or ADM alone, As(2)O(3) combined with ADM could increase the apoptosis rate of lymphoma cells with obvious difference (P<0.05). Semi-quantitive and RT-PCR showed that the expression of mutant p53 in As(2)O(3) and ADM alone and combined groups was obviously less than that in the control (P<0.05). After the treatment with 1 micromol/L and 2 micromol/L As(2)O(3), the fluorescene density in the Raji cells was 18.53 and 18.12, 0.056 and 0.023 times increase respectively.There was no difference (P>0.05). CONCLUSION As(2)O(3) and ADM alone or combined can inhibit the proliferation, induce cell apoptosis, and downregulate the expression of mutant p53 in vitro. As(2)O(3) combined with ADM has synergistic anti-lymphoma cell effect in vitro. As(2)O(3) has no significant effect on the concentration of ADM on the Raji cells, but can enhance the chemosensitivity of Raji cells, and its mechanism may be that it can downregulate the expression of mutant p53.
Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Arsenic Trioxide ; Arsenicals ; pharmacology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Doxorubicin ; pharmacology ; Drug Synergism ; Humans ; Lymphoma ; pathology ; Oxides ; pharmacology

Objective:To investigate the effect of long non-coding RNA (lncRNA) H19 regulating miRNA-675 (miR-675) and phosphatase and tensin homologue-deleted chromosome ten gene (PTEN) on the cell proliferation of glioma.Methods:Glioma cell lines U87-MG and U251 were chosen. The siRNA online design tool wad used to design small interfering RNA (siRNA) targeting H19. U87-MG and U251 cell lines with the stable knockdown of H19 were constructed (the stable knockdown of H19 group), and the cells randomly transfected with siRNA plasmid were taken as the control group, and normal cultured cells were treated as the blank group. Additionally, miR-675 and control microRNA were transfected into U87-MG and U251 with the stable knockdown of H19 (the overexpressing miR-675 group and the corresponding control group). Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the relative expression levels of miR-675 and H19 in each group; the methyl thiazolyl tetrazolium (MTT) assay was used to detect the cell proliferation ability; the dual luciferase reporter gene assay was used to verify the targeting relationship between miR-675 and PTEN; Western blot was used to detect the relative expression level of PTEN protein.Results:The MTT assay results showed that the proliferation ability of U87-MG and U251 cells in the stable knockdown of H19 group was lower than that of the corresponding control group; and the differences in cell proliferation ability of all the groups after 48 h of culture were statistically significant (all P < 0.05). qRT-PCR detection results showed that the relative expression level of miR-675 in U251 cells in the stable knockdown of H19 group and the corresponding control group was 0.329±0.009 and 1.043±0.087, respectively, and the difference was statistically significant ( t = 14.15, P < 0.001); the relative expression level of miR-675 in U87-MG cells in the stable knockdown of H19 group and the corresponding control group was 0.299±0.009 and 1.027±0.106, respectively, and the difference was statistically significant ( t = 11.85, P < 0.001); the relative expression level of miR-675 in U87-MG and U251 cells in the stable knockdown of H19 group was lower than that of the corresponding control group. The dual luciferase reporter gene assay verified that miR-675 could bind to the 3'-UTR of PTEN. Western blot detection results showed that the relative expression level of PTEN protein in U87-MG and U251 cells in the stable knockdown of H19 group was higher than that of the corresponding control group and the blank group; in the U87-MG and U251 cells in the stable knockdown of H19 group, the relative expression level of PTEN in the overexpressing miR-675 group was lower than that of the corresponding blank group and the control group. In the U87-MG and U251 cells in the stable knockdown of H19 group, the cell proliferation ability of the overexpressing miR-675 group was higher than that of the corresponding blank group and the control group; the differences in cell proliferation ability of all the groups after 48 h of culture were statistically significant (all P < 0.05). Conclusions:lncRNA H19 may regulate the cell proliferation of glioma cells through the miR-675-PTEN signaling pathway.