Growth Inhibitory Effects of Garlic Polysaccharide on Human HepG2 Cells

[Objective] The growth inhibitory effects of garlic polysaccharide(GPS) on human Hep G2 cells were evaluated in this paper. [Method] Hep G2 cells were treated with GPS for 48 h for morphology assay by transition electron microscope. Anti-proliferative effects with the same treatment for 24 hand 48 h were assayed by MTT method.Cell cycle distribution and apoptosis assay of treated cells were performed in flow cytometry. [Result] The results showed that GPS enhanced growth inhibitory effect on Hep G2 cells in a time-and dose-dependent manner. PI(Propidium iodide)/Annexin V staining analyzed by FCM(flow cytometry) demonstrated that GPS has a cytotoxic effect on tumor cells. Cell cycle arrest of Hep G2 treated with GPS occurred in G2 phase. [Conclusion] This study suggests that GPS could exert an antitumor effect and could be used as a therapeutic agent for live cancer.

THE LOCALIZATION OF ADRENOMEDULLIN IN RAT KIDNEY TISSUE AND ITS INHIBITORY EFFECT ON THE GROWTH OF CULTURED RAT MESANGIAL CELLS

OBJECTIVE: To observe the localization of adrenomedullin (AM) in rat kidney tissue and its inhibitory effect on the growth of cultured rat mesangial cells (MsC). METHODS: A monoclonal antibody against AM developed by our laboratory was used to detect the localization of AM protein in rat kidney tissue by avidin-biotin complex immunohistochemistry. The expressions of AM and its receptor CRLR mRNA on cultured glomerular epithelial cells (GEC) and MsC were investigated by Northern blot assay, and the possible effect of AM secreted by GEC on MsC proliferation was observed using [3H]thymidine incorporation as an index. RESULTS: A specific monoclonal antibody against AM was succesfully developed. AM was immunohistochemically localized mainly in glomeruli (GEC and endothelial cells), some cortical proximal tubules, medullary collecting duct cells, interstitial cells, vascular smooth muscle cells and endothelial cells. Northern blot assay showed that AM mRNA was expressed only on cultured GEC, but not on MsC, however, AM receptor CRLR mRNA was only expressed on MsC. GEC conditioned medium containing AM can inhibit MsC growth and AM receptor blocker CGRP8-37 may partially decreased this inhibitory effect. CONCLUSION: AM produced by GEC inhibits the proliferation of MsC, which suggests that AM as an important regulator is involved in glomerular normal physiological functions and pathologic processes.

Preparation and Inhibitory Effects of 20(S)-Ginsenoside Rh_2 on Hep-A-22 Cells

A modified method of preparing 20（S）-ginsenoside Rh2（G-Rh2） and the inhibitory effect of 20（S）-ginsenoside Rh2 on Hep-A-22 cells were investigated. The total saponins and strong alkali were dissolved in glycerol at the atmospheric pressure, and the degradation was performed at a high temperature. After G-Rh2 had been isolated and purified, MTT（methyl thiazolyl tetrazolium） assay was applied to evaluating the effect of 20（S）-ginsenoside Rh2 on the cells viability and morphological changes were observed. It was shown that 20（S）-ginsenoside Rh2 can reduce Hep-A-22 cells viability in dose-dependent manner and the cells took on cell shrinkage, membrane blebbing, chromosomal condensations, especially under the higher concentrations of it. In conclusion, 20（S）-ginsenoside Rh2 can be prepared effectively that not only decreases viability but also induces the apoptosis of Hep-A-22 cells.

The effect of endogenous transforming growth factor β_1 on the growth of bladder cancer cells in vitro

Objective To investigate the influence of endogenous transforming growth factor β1(TGFβ1) on the cell cycle regulation and proliferation of bladder cancer. Methods A constructed replication defective retroviral vector pRevTβ-AS, which carried antisense RNA of TGFβ1.was transfected to a bladder cancer cell line EJ. The proliferation and clone-formation of transferred cells were observed in vitro,and the alteration of cell cycle was also detected by flow cytometric analysis. Results TGFβ1 antisense RNA was transferred into EJ cell and expressed efficiently. After the inhibition of target gene expression in EJ cells, the reduced growth and clone-formation rates were demonstrated, and the proliferative indexes were decreased by 12 % . The ratios of GO and G1 stage cells to June 2003 Vol12 No2 the antisense RNA-transfected EJ cells were increased, simultaneously,the ratio of S stage cells to the antisense RNA-transfected EJ cells ratios were decreased, compared with the control group. Conclusion The

Effect of temsirolimus on bladder cancer cells in vitro and in vivo

Objective To examine the effects of temsirolimus, an inhibitor of mammalian target of rapamycin,on bladder cancer cell lines T24 and BIU-87 in vitro and in vivo for purpose of evaluating the probability of mTOR targeted therapy for bladder cancer. Methods After

Anti-tumor effects of p53N15-based fusion peptide in the transfected H1299 lung cancer cells

Objective Loss-of-function mutation of p53,a tumor suppressor gene,is an important mechanism for the development of human cancers. In this study we tried to transfect p53N15-based fusion peptide into H1299,a lung cancer cell line,and evaluate the anti-tumor effects of the fusion peptide. Methods Adeno-associated virus (AAV) vectors were used for transfecting p53N15 fusion peptide into p53-null lung adenocarcinoma H1299 cells.

Macrophage migration inhibitory factor regulates proliferation of gastric cancer cells via the PI3K/Akt pathway

AIM:To investigate the effects of macrophage migration inhibitory factor (MIF) on proliferation of human gastric cancer MGC-803 cells and expression of cyclin D1 and p27Kip1 in them,and further determine whether the effects are related to the PI3K/Akt signal transduction pathway. METHODS:Gastric cancer MGC-803 cells were cultured and then treated with 50 μg/L recombinant human MIF (rhMIF) with and without a PI3K inhibitor,LY294002 (25 μmol/L). MTT assay was used to detect the prolifer-ation of MGC-803 cells. Cell cycle was detected by flow cytometry. Expression of cyclin D1 and p27Kip1 mRNA was by reverse transcription-polymerase chain reaction. Protein expression of phosphorylated Akt (p-Akt),Akt,cyclin D1 and p27Kip1 was examined by immunocyto-chemistry and Western blotting. RESULTS:rhMIF signifi cantly stimulated the prolifera-tion of MGC-803 cells and cell cycle progression from G1 phase to S phase in a concentration-and time-de-pendent manner. After the MGC-803 cells were treated with rhMIF for 24 h,the expression of cyclin D1 was signifi cantly up-regulated compared with the cells not treated with rhMIF at both mRNA and protein levels(0.97 ± 0.02 vs 0.74 ± 0.01,P = 0.002; 0.98 ± 0.05 vs 0.69 ± 0.04,P = 0.003). The p27Kip1 was down-regulated but only statistically significant at the protein level. rhMIF significantly increased the expression of p-Akt,which reached the peak at 30 min,but did not affect the expression of Akt. However,LY294002 inhibited all the effects of rhMIF.CONCLUSION:Macrophage MIF increases the proliferation of gastric cancer cells,induces the expression of cyclin D1 at the transcriptional level and inhibits the expression of p27Kip1 at the post-transcriptional level via the PI3K/Akt pathway.

Effects of MIF on proliferation,migration,and STAT1 pathway of colon cancer cells

Objective This study aimed to investigate how macrophage migration inhibitory factor(MIF)regulates the interaction of signal transducer and activator of transcription 1(STAT1)with CD74,and affects colon cancer proliferation and invasion.Methods After transfecting MIF small interfering RNA into the SW480 cell line,the expression of STAT1 and CD74 mRNA was detected by qRT-PCR and western blotting.Transwell and MTT assays were performed to detect the colon cancer cell invasion and proliferation ability.Co-immunoprecipitation was used to detect the interaction between CD74 and STAT1 proteins in the treated and control groups.Results The cellular biological assays(MTT and Transwell)showed that the proliferation and invasion ability of colon cancer cells decreased after MIF knockdown;the results showed significant statistical difference(P<0.05).The results of the co-immunoprecipitation assay suggested that MIF knockdown in colon cancer cells could inhibit the binding of CD74 and STAT1 proteins;statistical difference was observed between the two groups(P<0.05).Conclusion MIF can increase the proliferation and invasion of colon cancer cells by promoting the combination of CD74 and STAT1.

Identification of the Diterpenoids Produced by Endophytic Fungus of Torreya fargesii and Its Inhibitory Effect on Hela Cells

[Objectives] The purpose of this study is to dissociate endophytic fungus producing diterpenoids from Torreya fargesii tissue and examines its inhibiting effect on tumor cells. [Methods]Plant endophytes were isolated and purified to study their resistance to Gram-positive( G+) and Gram-negative bacteria( G-). High performance liquid chromatography( HPLC) was used for analysis of the retention time,relative peak area and percentage content of its metabolite. By liquid chromatography-mass spectrometry( HPLC-MS),the material characteristic of the ion pair information of the metabolites was measured. The bacterial strain was also classified. [Results] The results showed that the secondary metabolites produced by the strain BP6 T3 possessed double resistance to G+and G-bacteria. The strain was identified as Penicillium sp by preliminary classification. Through HPLC analysis,the retention time of fermentation extracts was 12. 8 min with almost the same as the standard of taxol. According to the chromatograph,the relative peak area was 12 887. 11,the average relative percentage was about 15. 8%,and the content of taxol analogs in fermentation broth reached 16. 59 mg/L. The material characteristic of the formation of ion fragments of taxane analogues in metabolic extracts was identical to that of the taxol standard determined by HPLC-MS. It can be initially determined that strain BP6 T3 can produce taxane compounds. Taxol substance produced by this strain had obvious inhibitory effect on Hela cells with the concentration increasing. Different precursors had a significant effect on the production of paclitaxel metabolites in this strain. L-phenylalanine was used as the precursor and the yield increased most,with an increase rate of 425. 7%. [Conclusions] The strain is expected to be used for mass production in antitumor drug taxol.

Inhibitory Effects of Bio-Energy Therapies on Cancer Growth——An overview of recent laboratory studies in the U.S.and its implications in cancer treatment

Background:Bioenergy therapies(such as Qigong,Reiki,Yoga,Pranic healing,and Therapeutic touch)have reported benefits for cancer patients,but few randomized control trials were done to verify their efficacy.It is believed that laboratory study of inhibito- ry effects of bio-energy therapies on cancer growth may lead to an understanding of the true efficacy of bio-energy and create a foun- dation for future clinical trials.Methods:Typical in-vitro study involved randomly dividing lab-prepared cancer cells into different groups with one being treated by bio-energy therapy and one or more as control groups.Sometimes,controls were treated by a sham healer.Typical in vivo study involved injecting or implanting cancerous cells into mice,then randomly dividing them into various groups.The control could be either non-treatment or sham treatment;the outcomes include tumor size or survival time.Results:Most studies demonstrated some inhibitory effects ofbioenergy therapies on the growth of cancer cells in comparison with control.The in vivo studies reported that the bio-energy treated group had significantly slower tumor growth or longer survival lives than those in the control.One study reported survival with a normal life cycle instead of dying in 3 weeks,and cancer-infected mice developed immune response to the same breast cancer.However,researchers are confronted with methodological challenges in choosing appropriate con- trois,minimizing contamination,and replicating study outcomes.Conclusion:Encouraging evidence suggests bioenergy may have inhibitory effects on cancer growth,or prolong the life of cancer-infected animals,although improvement is needed in research design and replication of the findings.Bioenergy for cancer treatment is an area that is often neglected by mainstream medicine and research, and it should be seriously examined and considered as an important supplement to conventional cancer treatment.

Inhibitory effect of parvovirus H-1 on the formation of colonies of human hepatoma cell line in vitro and its tumors in nude mice

The inhibitory effect of parvovirus H-1 on the colonyforming ability in vitro of QGY-7703, a cultured human hepatoma cell line, and on the formation and growth of its tumors in nude mice was studied. With higher multiplicity of infection (MOI) of H-1 given, survival of the QGY-7703 cells was found to be decreased. H-1 DNA amplification level at 30 h postinfection(p.i.) was detected to be 7.4 times higher than that at 2 h by dispersed cells assay, while the cells were delayed to enter into S phase.Plaques were formed in the indicator cells (new-born human kidney cell line, NBK) by progeny H-1 virus particles released from the infected QGY-7703 cells by infectious cell center assay. The formation of tumors in nude mice by QGY-7703 cells which were injected s c at 2 h postinfection was observed to be prevented in 2 groups with given MOI 25 and 50. The tumor growth of MOI 10 group occurred at a lower exponential rate than that of control,after a 20 d latent period. It was evident that parvovirus H-1 exhibited a direct inhibitory effect on the formation and growth of human hepatoma cells in vivo as well as in vitro.

Inhibitory effect of survivin-shRNA on A431 cutaneous squamous cell carcinoma

Objective:To observe the effect of survivin-shRNA on A431 cutaneous squamous cell carcinoma(SCC)and explore the molecular biological mechanism of nuclear factorκB(NF-κB)in the inhibition of survivin-shRNA on cutaneous SCC.Methods:Survivin-shRNA adenovirus vector was constructed to screen out the best interference sequence.Nude mice were subcutaneously inoculated with the cultured A431 cell suspension to duplicate A431 transplanted tumor models.These mice were randomly divided into the blank control group,the rAd-EGFP negative control group,the rAd-survivin-shRNA transfection group and the Res positive control group,with 5 mice in each group.The corresponding reagents were injected into the tumors.All the mice were sacrificed on the 20th day.The tumor tissues were isolated,with tumor volume and tumor weight measured,the tumor growth curves were accordingly plotted and the tumor inhibition rate was consequently calculated.Hematoxylin-eosin(HE)staining was used to observe the cellular morphology of the tumors.TUNEL was applied to the detection of cell apoptosis.Western blot was applied to the detection of the expression of Survivin,inhibitor of NF-κB(IκB),P65,P53 and Caspase-3.Results:As to the transplanted tumors,tumor volume and tumor weight were decreased in nude mice in the rAd-survivinshRNA transfection group and the Res positive control group,in comparison with the blank control group and the rAd-EGFP negative control group,the differences were of statistical significance(p<.05);The results of TUNEL showed that the apoptosis rates were significantly increased in the rAd-survivin-shRNA transfection group and the Res positive control group,in comparison with the blank control group and the rAd-EGFP negative control group,the difference was statistically significant(p<.05);In the rAd-survivin-shRNA transfection group and the Res positive control group,the microscopic observation showed a small amount of sparsely-distributed tumor cells,degenerative liquefactive necrosis,cancer cell shrinkage and round-shape,and karyopycnosis;The expressions of Survivin and P65 proteins were decreased in the rAd-survivin-shRNA transfection group and the Res positive control group,in comparison with the blank control group and the rAd-EGFP negative control group,the differences were statistically significant(p<.05),while the expressions of IκB,P53 and Caspase-3 proteins were significantly increased,in comparison with the blank control group and the rAd-EGFP negative control group,the differences were statistically significant(p<.05).Conclusions:Survivin-shRNA can inhibit the growth of the transplanted tumors in cutaneous SCC nude mice,one of the mechanisms is to promote the apoptosis of tumor cells and inhibit the growth of SCC transplanted tumors by inhibiting the NF-κB signaling pathway and then activating the tumor suppressor gene P53.

Metabolic alterations in cancer cells and therapeutic implications

Cancer metabolism has emerged as an important area of research in recent years.Elucidation of the metabolic differences between cancer and normal cells and the underlying mechanisms will not only advance our understanding of fundamental cancer cell biology but also provide an important basis for the development of new therapeutic strategies and novel compounds to selectively eliminate cancer cells by targeting their unique metabolism.This article reviews several important metabolic alterations in cancer cells,with an emphasis on increased aerobic glycolysis (the Warburg effect) and glutamine addiction,and discusses the mechanisms that may contribute to such metabolic changes.In addition,metabolic alterations in cancer stem cells,mitochondrial metabolism and its influence on drug sensitivity,and potential therapeutic strategies and agents that target cancer metabolism are also discussed.

Seeking the Source of Transience for a Unique Magnetic Field Pattern That Completely Dissolves Cancer Cells <i>in Vitro</i>

Purpose: Exposure to a particular pattern of weak (~3 to 5 μT) magnetic fields produced by computer-generated point durations within three-dimensions completely dissolved malignant cancer cells but not healthy cells. Biomolecular analyses and confocal microscopy indicated excessive expansion followed by contraction contributed to the “explosion” of the cell. However, after months of replicable effects, the phenomenon slowly ceased. Considering the potency of the complete dissolution of cancer cell lines after 5 days of 6.5-hour daily exposures and the implications for human treatment, the potential source of the disappearance of the effect was pursued by summarizing all of the 50 experiments and assessing the likely etiologies. Materials and Methods: B16-BL6, MDAMB 231 and MCF7 malignant cells and HSG, a non-malignant cell line, were exposed to a sham-field condition or to a specific pattern of computer-generated magnetic fields produced from converting different voltages, each with point durations of 3 ms to 3-D magnetic fields. Conclusion: The specific serial presentation of the two field patterns (one frequency modulated;the other amplitude and frequency modulated) completely dissolved malignant cells but not normal cells within a “zone” within the exposure volume at the conjunction of the three planes of the applied magnetic fields. The affected cells underwent massive melanin production, expansion, contraction and “beading” of submembrane actin structures before fragmentation within this zone. However, this powerful all-or-none phenomenon may have been disrupted by moving the cells, excess mechanical agitation during exposure, or non-optimal point durations of the field parameters. Indirect effects from communication signals (WIFI) through line currents that operated the incubators could not be excluded.

Correlation of serum GDF-15 and MIF contents with the malignant behaviors of cancer cells in patients with NSCLC

Objective:To study the correlation of serum GDF-15 and MIF contents with the malignant behaviors of cancer cells in patients with NSCLC.Methods: Patients with non-small cell lung cancer who underwent surgical resection in Kashgar Prefecture First People's Hospital in the Xinjiang Uygur Autonomous Region between January 2015 and November 2017 were selected as lung cancer group for the research, and healthy volunteers who received physical examination in Kashgar Prefecture First People's Hospital in the Xinjiang Uygur Autonomous Region during the same period were selected as the control group. Serum was collected from the lung cancer group before surgery and from the control group during physical examination respectively to determine the contents of GDF-15 and MIF;lung cancer tissue and adjacent tissue were collected from lung cancer group after surgery to determine the expression of tumor suppressor genes, proliferation genes and invasion genes.Results:Serum GDF-15 and MIF contents of lung cancer group were significantly higher than those of control group;TCF21, Bax, GRPC5A and PTEN mRNA expression in lung cancer tissue were significantly lower than those in the adjacent tissue whereas Bcl-2, AQP4, c-myc, CyclinD1, SIRT1, CatL, MMP9, N-cadherin and Vimentin mRNA expression were significantly higher than those in adjacent tissue;serum GDF-15 and MIF contents of patients with lung cancer were negatively correlated with TCF21, Bax, GRPC5A and PTEN mRNA expression, and positively correlated with Bcl-2, AQP4, c-myc, CyclinD1, SIRT1, CatL, MMP9, N-cadherin and Vimentin mRNA expression in lung cancer tissue.Conclusion:The abnormal increase of GDF-15 and MIF in patients with NSCLC is closely related to the abnormal proliferation and invasion of cancer cells.

In Vitro and In Vivo Inhibitory Effect of the Combination of Wenxia Changfu Formula(温下肠腑方) with Cisplatin in Non-Small Cell Lung Cancer

Objective： To observe the effect of the combination of Wenxia Changfu Formula （温下肠腑方, WCF） with cisplatin （CDDP） on inhibiting non-small cell lung cancer （NSCLC） in vitro and in vivo and explore its mechanism from its effect on cell cycle. Methods： In vitro, WCF-containing serum was prepared and the rhubarb bl, emodin, and aconitine were detected qualitatively by high-performance liquid chromatogram （HPLC）. A549 cell lines were treated with blank control （dimethyl sulfoxide）, normal serum, normal serum with CDDP （1.25, 2.5, and 5.0 μg/mL, respectively）, WCF-containing serum plus different doses of CDDP （1.25, 2.5, and 5.0 μ g/mL, respectively）. The inhibitory effect was detected by 3-（4,5）-dimethylthiazo（-z- yl）-3,5-diphenylterazolium bromide （MI-I）. The cell cycle was detected by flow cytometry. The protein and mRNA expressions of cyciin D1, proliferating cell nuclear antigen （PCNA）, retinoblastoma （Rb）, and p16 were observed with immunofluorescence and RT-PCR, respectively. In vivo, nude mice xenograft model was established and grouped into the control, CDDP, WCF, and combination groups. The combination＇s inhibition of tumor growth and influence on the weight, spleen, and thymus gland were observed. Results： The inhibitory rate of the combination against A549 cell lines excelled the CDDP alone significantly （P〈0.05）; the combination showed a synergism inhibitory effect （Q=1.19）. Compared with the monotherapy, the combination increased the cell percentage in G0/G1 phase and decreased the cell percentage in S phase significantly （P〈0.05）; the protein and mRNA expressions of cyclin D1, PCNA, and Rb were significantly reduced; the protein and mRNA expressions of p16 were significantly enhanced. Compared with the monotherapy, the combination inhibited the tumor growth significantly in vivo and reduced the weight of tumor （P〈0.05）; compared with the CDDP group, the spleen and thymus gland index of the combination group were enhanced significantly （P〈0.05）. Conclusions： The combination of WCF with CDDP significantly inhibited the A549 cell lines proliferation in vitro and the growth of the tumor in vivo; it inhibited effectively the atrophy of the immune organ caused by chemotherapy. The combination inhibited overproliferation of A549 cell lines by arresting the Go/G1 phase of cell cycle and affecting the protein and mRNA expressions of cell cycle-related proteins, cyclin D1, etc.

EFFECTS OF HYPOXIC ENDOTHELIAL CELL CONDITIONED MEDIUM ON PROLIFERATION AND COLLAGEN SYNTHESIS OF SMOOTH MUSCLE CELLS AND INHIBITORY EFFECTS OF RADIX SALVIAE MILTIORRHIZAE

The effects of hypoxic endothelial cell conditioned medium (HECCM) on proliferation and collagen synthesis of cultured porcine pulmonary arterial smooth muscle cells (PASMCs) were studied by 3H-thymidine (3H-TdR) and 3H-proline incorporations, image analysis for determination of DNA content and colorimetric assay using MTT, and the inhibitory effects of radix salviae miltiorrhizae (RSM) on them were also investigated. The results showed that HECCM could induce enhancement of the enzymatic activity of mitochondria, increase of the nucleic DNA content and increases of the 3H-TdR and 3H-proline incorporations in PASMCs. The 3H-proline incorporation in PASMCs cultured in HECCM was 1.83 times as much as that cultured in normoxic endothelial cell conditioned medium (NECCM). Compared with the control, Chinese herb medicine RSM could inhibit the proliferation of PASMCs cultured in HECCM and decrease the 3H-prolinc incorporation in PASMCs cultured in both HECCM and NECCM (P< 0.001). However, RSM had no ef fects on the nucleic DNA content and 3H-TdR incorporation into DNA of PASMCs cultured in NECCM. It suggests that hypoxia may stimulate the endothelia to synthesize and secrete some cytokines which can stimulate the proliferation and the synthesis of collagen of PASMCs and RSM can inhibit this process.

Effects of human microRNA-181a-5p on proliferation and migration of gastric cancer cells

Objective To preliminarily explore the effects of human microRNA-181a on migration of gastric cancer cells and its mechanism.Methods The expression of miRNA-181a-5p in gastric cancer cell line GC9811 and peritoneal high metastasis gastric cancer cell line GC9811-P were tested by quantitative real-time polymerase chain reaction(qRT-PCR).GC9811 cell line was

Dietary Daidzein Enhances Antiapoptotic Effect of 17β-Estradiol (E_2) on Breast Cancer MCF-7 Cells

Objective： To investigate whether dietary daidzein interact with endogenous 17β-Estradiol （E2） to give rise to additive or inhibitory effects on proliferation and apoptosis in breast cancer cells. Methods： Cell cycle distribution and apoptosis induction were analyzed by using flow cytometry when breast cancer cell lines MCF-7 were cotreated with daidzein （1, 5 μmol/L） and E2 （0.1-10 nmol/L） for 5 days. Whether daidzein could alter E2-modulated mRNA expression of estrogen receptor alpha （ERα）, estrogen receptor beta （ERI3） and ERβ-estrogen response element （ERE） dependent transcription was investigated by RT-PCR and luciferase induction assays. The effects of daidzein on E2-modulated expression of proapoptotic p53, bax and antiapoptotic bcl-2 at both mRNA and protein levels were also investigated by RT-PCR and Western blot. Results： Daidzein enhanced the antiapoptotic effect in an Ea dose-dependent manner, but had no effect on E2-induced proliferation. Daidzein antagonized E2-induced ERβ mRNA expression and ERβ-ERE dependent transcription. In addition, daidzein only antagonized E2-upregulated expression of p53 and bax, but had no effect on E2-upregulated expression of bcl-2. Conclusion： Daidzein enhances the antiapoptotic effect of E2 on breast cancer cells by inhibiting E2-mediated p53-bax proapoptotic pathway. These results suggest that dietary daidzein may enhance deleterious effect of endogenous E2 in hormone-dependent breast cancer.

ANTI-HUMAN LUNG GIANT CELL CANCER (PG) EFFECT OF HUMAN LAK CELLS IN VITRO AND IN NUDE MICE

Human LAK cells were prepared by culturing normal human peripheral blood mononuclear cells (PBMC) with or without rIL-2 and assayed for T cell surface markers as well as anti-tumor activity against PC in vitro and in nude mice. Although the percentages of T3, T4, and T8 positive cells in rIL-2-activated cells did not differ significantly from those of control cells in vitro, the former showed stronger cytotoxicity than control cells to PG tumor cells in vitro. In vivo, LAK cells completely inhibited the growth of PG tumor in nude mice, whereas PBMC control cells were to be of no effect. The anti-tumor effect of human LAK cells in nude mice may offer a useful model to study the role of human LAK cells against human tumor in vivo.