[Leukemic stem cell targeting therapy].
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Animals↗
Biomedical subjects
Xue-Yun Zhong
Publications and source records attributed to Xue-Yun Zhong.
Synergistic effect of cell differential agent-II and arsenic trioxide on induction of cell cycle arrest and apoptosis in hepatoma cells.
AIM: To illustrate the possible role of cell differential agent-II (CDA-II) in the apoptosis of hepatoma cells induced by arsenic trioxide (As(2)O(3)). METHODS: Hepatoma cell lines BEL-7402 and HepG2 were treated with As(2)O(3) together with CDA-II. Cell surviving fraction was determined by MTT assay; morphological changes were observed by immunofluorescence staining of Hoechst 33,258; and cell cycle and the apoptosis index were determined by flow cytometry (FCM). RESULTS: Cytotoxicity of CDA-II was low. Nevertheless, CDA-II could strongly potentiate arsenic trioxide-induced apoptosis. At 1.0 g/L CDA-II, IC(50) of As(2)O(3) in hepatoma cell lines was reduced from 5.0 micromol/L to 1.0 micromol/L (P<0.01). The potentiation of apoptosis was dependent on the dosage of CDA-II. FCM indicated that in hepatoma, cell growth was inhibited by CDA-II at lower concentrations (<2.0 g/L) primarily by arresting at S and G(2) phase, and at higher concentrations (>2.0 g/L) apoptotic cell and cell cycle arresting at G(1) phase increased proportionally. The combination of two drugs led to much higher apoptotic rates, as compared with the either drug used alone. CONCLUSION: CDA-II can strongly potentiate As(2)O(3)-induced apoptosis in hepatoma cells, and two drugs can produce a significant synergic effect.
Apoptosis↗
15d-PGJ2 inhibits cell growth and induces apoptosis of MCG-803 human gastric cancer cell line.
AIM: To investigate the influence of peroxisome proliferator-activated receptor gamma (PPARgamma) ligand, 15-deoxy-12, 14-prostaglandin J2 (15dPGJ2) on the proliferation and apoptosis of MCG-803 human gastric cancer cell lines. METHODS: Cell proliferation was measured by 3H-TdR assay. Apoptosis was determined by ELISA and TUNEL staining. Protein and mRNA level of bcl-2 family and COXs were measured by Western blotting and Northern blotting respectively. PGE2 production was examined by RIA. RESULTS: 15dPGJ2 inhibited cell growth and induced apoptosis of MCG-803 cells. The COX-2 and bcl-2/bax ratios were decreased following 15dPGJ2 treatment. The PGE2 production in supernatants was also decreased. These changes were in a dose-dependent manner. CONCLUSION: 15dPGJ2 may be a useful therapeutic agent for the treatment of gastric cancer.
Apoptosis↗
Synergistic effects of nimesulide and 5-fluorouracil on tumor growth and apoptosis in the implanted hepatoma in mice.
AIM: To compare the effect of nimesulide or/and 5-fluorouracil (5-FU) on tumor growth inhibition and apoptosis in mice with the implanted hepatoma and to observe their possible interactions. METHODS: The inhibitory effects on tumor growth was evaluated by inhibition rate. Apoptosis was assessed by the ultrastructural, flow cytometry features and the DNA ladder demonstrated by agarose gel electrophoresis. PGE(2) level was determined by radioimmunoassay. Expression levels of c-jun, c-fos and p53 were evaluated by western blotting. RESULTS: Nimesulide or 5-FU alone inhibited the growth of hepatoma, while a synergistic effect was observed for a combined use of both. More pronounced morphologic changes for tumor cell apoptosis and the DNA ladder were found for the latter treatment. Expression levels of c-jun and p53 were found to be elevated for the tumors from mice treated with nimesulide and 5-FU comparing to those with either of them, but a reduced PGE(2) level was observed only for the treatment with nimesulide. No change was detected on c-fos expression. CONCLUSION: Nimesulide and 5-FU appear to have synergistic effects for the growth inhibition and apoptosis induction. Both were found to be overexpressed in p53 and c-jun proteins, rather than that of c-fos, associations with the resulted apoptosis.
Animals↗
[Relationship between tumor necrosis factor genetic polymorphisms and acute lymphocytic leukemia].
BACKGROUND & OBJECTIVE: Acute lymphocytic leukemia(ALL), which is sensitive to tumor necrosis factor (TNF) is one of hematological malignances derived from lymphoid tissue. Genetic polymorphisms in the tumor necrosis factor (TNF) locus can affect transcription and expression of TNF genes. This study was designed to investigate the relationship between -308 bp polymorphism in tumor necrosis factor-alpha(TNFalpha) gene and +252 bp in lymphotoxin-alpha(LTalpha) gene and the pathogenesis, clinical course, and outcome of ALL. METHODS: The single base mutation polymorphism in TNFalpha gene and LTalpha gene were analyzed among 29 Chinese patients with ALL and 72 normal controls using polymerase chain reaction (PCR)-restrictive fragment length polymorphism (RFLP). The clinical data were collected and survival analysis was performed. RESULTS: The difference of distribution of genotypes, alleles of TNFalpha(-308), LTalpha(+252), and TNF/LT polymorphic extended haplotypes between the ALL patients and control group were not statistically significant (P >0.05). In patients, no statistically significant association was found between the presence of a given TNF/LT haplotype status and clinical characters such as sex, white blood cell (WBC) counts, central nervous system involvement, and the response to therapy(P >0.05). The estimated 1-year overall survival rates in the groups of patients carrying high-risk and low-risk haplotypes were not statistically significant (P >0.05) using Kaplan-Meier method. In multivariate Cox regression models the TNF/LT haplotype status was not found to be a risk factor for outcome (P >0.05). CONCLUSION: These data suggest that genetic polymorphisms in the TNFalpha(-308) and LTalpha(+252) are not crucial in the pathogenesis, clinical course, and outcome of ALL patients.
Adolescent↗