[Effect of emodin on induction of apoptosis in jurkat cells and its possible mechanisms].

The aim of study was to investigate the effect of a traditional Chinese medicine, emodin, on proliferation and apoptosis in T lymphocytic leukemic cell line Jurkat and its mechanisms. Cell proliferation inhibition was detected by MTT assay. Cell apoptosis was measured by DNA ladder and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay.

[Effect of bcl-2 siRNA on apoptosis of Burkitt's lymphoma cell line CA46].

The aim of this study was to investigate the effect of bcl-2 siRNA on bcl-2 gene expression and apoptosis of lymphoma cell line CA46. A siRNA was designed and synthesized. Then siRNA was transfected into CA46 cells by cationic liposome.

[Emodin induces leukemic HL-60 cells apoptosis probably by inhibiting Akt signal pathway].

This study is to investigate the effect of emodin on inducing human myeloid leukemia cell line HL-60 apoptosis and the role of Akt signal pathway in the apoptosis. HL-60 cells were exposed to various dosages of emodin. MTT assay was used to detect HL-60 cell proliferation.

[Inhibitory effects of emodin on drug-resistant HL-60/ADR cell proliferation and its induction of apoptosis].

The study was aimed to investigate the effects of emodin on the proliferation and apoptosis of adriamycin-resistant HL-60/ADR cells, and to explore the underlying mechanism. The cell viability and colony formation were detected by MTT assay and colony formation assay respectively. Apoptotic cells were tested by means of cell cycle analysis, mitochondrial transmembrane potential levels, caspase-3 activity detection, Annexin V FITC/PI staining and TUNEL labeling.

[A novel bcl-2 antisense oligodeoxynucleotide F951 increases sensitivity of HL-60 cells to Ara-C].

To investigate whether F951, a novel bcl-2 antisense oligodeoxynucleotide, increases the sensitivity of HL-60 cells to Ara-C, HL-60 cells were cultured with F951 in different doses alone or with F951 combined with low-dose Ara-C; the proliferation of HL-60 cells was assayed by MTT and trypan blue exclusion test; expression of Bcl-2 protein and its mRNA were measured by FACS and RT-PCR, respectively; the apoptotic cells were detected by DNA ladder and TUNEL assay. The results showed that F951 combined with low dose Ara-C revealed stronger effects in the aspects of inhibiting the HL-60 cells proliferation than in different doses of F951 alone or Ara-C alone. HL-60 cells treated with F951 + Ara-C had significantly lower trypan blue exclusion rate than that treated with Ara-C alone.

[New insight into the mechanism of p53 inducing leukemia cell apoptosis].

Objective: To investigate the expression changes of intrinsic cytokines TGF-beta(1) and TNF-alpha, telomerase activity and bcl-2 during ongoing apoptosis of HL-60 and K562 cells induced by p53.

Methods: pN53cG (Val135), a temperature sensitive p53 mutant, which behaved like wild type p53 (wt-p53) at 32.5 degrees C, were introduced into p53-null HL-60 and K562 cells respectively by lipofectin.

[The effect of anti-bcr-abl hammerhead ribozyme on bone marrow purging].

To study effects of a hammerhead ribozyme on chronic myelogenous leukemia (CML) cells and bone marrow purging in vitro, a bcr-abl specific ribozyme gene was introduced into CML and normal bone marrow cells using retroviral transduction. The effects of the ribozyme on primary cells from CML patients were detected by hematopoietic progenitor cell assays, flow cytometry and immunocytochemical methods. Then a model of remission was built up, and the effects of ribozyme on bone marrow purging were detected by leukemia colony assay and nest-PCR after transduction of this model by using the ribozyme.

[Bcl-2 antisense oligonucleotides suppress HL-60 cell growth in a SCID mouse mode].

Objective: To study the effects of bcl-2 antisense phosphorothioate oligonucleotides (ASPO) on suppression of HL-60 cell growth in SCID mice and to investigate the feasibility of purging leukemia cells plus bcl-2 ASPO used in vitro.

Methods: 1 x 10(7) viable HL-60 cells were treated with 10 micro mol/L bcl-2 ASPO seven days before the intraperitoneal (IP) inoculation to the SCID mice, Treatment with sense oligonucleotides (SPO) was similar as for the controls. 35 days after the inoculation, all the SCID mice of both groups were sacrificed and their peripheral blood, bone marrow, liver and spleen were examined using half nested RT-PCR and histopathology for detecting the appearance and distribution of the HL-60 cells treated beforehand with antisense or sense oligonucleotides respectively.

[Effect of endogenous TGF-beta1 and TNF-alpha on the As(2)O(3) inducing apoptosis of HL-60 cells].

Objective: To study the effect of endogenous TGF-beta(1) and TNF-alpha on As(2)O(3) inducing apoptosis of HL-60 cells.

Methods: The expressions of endogenous TGF-beta(1) and TNF-alpha in apoptotic HL-60 cells induced by As(2)O(3) were assayed by RT-PCR, quantitative RT-PCR, ELISA, DNA fragmentation and TUNEL. The effect of TGF-beta(1) and TNF-alpha antisense phosphorothioate oligodeoxynucleotides (PSODNs) on As(2)O(3) inducing apoptotic HL-60 cells was further studied.

[c-myc Antisense Oligodeoxynucleotides Induce Apoptosis of Human Myeloid Leukemia Cell Line HL-60].

In order to study the effects of c-myc antisense phosphorothioate oligodeoxynucleotide in inducing apoptosis of HL-60 cells, the expression of c-myc mRNA was determined by RT-PCR, the morphologic signs of apoptotic cells were observed by transmission electron microscopy, the proportion of apoptotic cells was detected by flow cytometry, and the DNA fragments were analysed by agarose gel electrophoresis. Results of RT-PCR showed marked decrease of c-myc mRNA expression in AspoI and II treated cells. The level of c-Myc protein was decreased 23.

[Effects of Exogenous Wild-Type p53 Gene on K562 Cells].

To investigate the effects of wt-p53 gene on proliferation and differentiation of K562 cells and to explore the feasibility of wt-p53 in leukemia gene therapy, pC53-SN(3), containing wt-p53 cDNA, and temperature-sensitive p53 mutant pN53cG(Val135) which behaved like wt-p53 at 32.5 degrees C, were introduced into p53-null K562 cells respectively by lipofectin mediated DNA transfection. In the presence of G418, K-SN(3) and K-pN53cG clones expressing P53 protein were selected.

[Effects of SCL antisense ooligonucleotides on K562 and CEM cell lines].

The stem cell leukemia (SCL) gene is a new oncogene related with leukemogenesis. To explore the effects of antisense oligonucleotides of SCL on leukemic cells, SCL antisense phosphorothioate oligodeoxynucleotides (AS-PS-ODN) were used to treat K562 and CEM leukemic cell lines to observe the effects on proliferation, differentiation, apoptosis and SCL mRNA expression in the cells. The results showed that incubation of K562 or CEM cells with AS-PS-ODN at different concentrations led to inhibition of cell proliferation, and the inhibitory effects varied with the incubation time.

[Effect of p53 gene on telomerase activity and hTERT gene expression in HL-60 cells].

To investigate the change of telomerase activity and human telomerase reverse transcriptase (hTERT) gene expression in HL-60 cells transfected with wild type p53 gene, wild type p53 gene was introduced into HL-60 cells by Lipofectin transfection. Apoptosis was analyzed by TUNEL assay. Telomerase activity and the level of hTERT mRNA were detected by telomeric repeat amplification protocol (TRAP)-ELISA and RT-PCR, respectively.