In vitro cytotoxicity assay of Fucoidan extracted from Turbinaria conoides against cancer cell lines MCF7, A549, and normal cell line L929

Abstract The main aim of the study is to quantify the cytotoxic property of the Fucoidan extracted from the Turbinaria conoides using the MTT assay with the standard fucose. Fucoidan was extracted using the soaked water method and it was determined using the HPLC procedure the obtained Test sample Fucoidan extracted from the Turbinaria conoides and standard fucose was subjected to the cytotoxicity assay against the MCF7 Human breast cancer cell line, A549 lung cancer cell line, and L929 normal mouse fibroblast cell line. From the results it was found that the Test sample showed good IC50 value for MCF7 cell line then A549 with an increasing concentration 24 hours incubation at 37°C The IC50 for MCF7 was 115.21 µg/ml and A549 396.46µg/ml and the Fucoidan extract was checked for its cytotoxicity against the normal mouse fibroblast cell line L929, Fucoidan was found non-lethal to the L929 mouse fibroblast normal cell line. Standard fucose also gave a significant result towards MCF7 and against the L929. This indicates that the Fucoidan extracted from Tubinaria conoides shows better anticancer potential in it. Hence its application can be further extended in the pharmacological fields.

Exploration of organoid in breast cancer related research / 生物工程学报

Breast cancer is the most common cancer in women. At present, the in vivo model and traditional cell culture are mainly used in breast cancer researches. However, as high as 90% clinical trials are failed for drugs explored by the above two methods, due to the inherent species differences between humans and animals, as well as the differences in the tissue structure between organs and cells. Therefore, organoid three-dimensional culture is emerging. As a new tumor research model, organoid, a three-dimensional cell complex with spatial structure, has broad application prospects, such as precision medicine, organ transplantation, establishment of refractory disease model, gene therapy and drug research and development. Therefore, organoid is considered as one of the ideal carriers for life science research in the future. Breast cancer, a heterogeneous disease with complex phenotypes, has a low survival rate. Breast cancer organoid can reproduce many key features of human breast cancer, thus, the construction of organoid biological library of breast cancer will provide a new platform for studying the occurrence, development, metastasis and drug resistance mechanism of breast cancer. In this review, we systematically introduce the culture conditions of organoids and their application in breast cancer related research, and the application prospect of organoids.

Effect of hypoxia on epithelial growth factor receptor expression and cell apoptosis of breast cancer and cervical cancer xenografts in nude mice / 中华放射肿瘤学杂志

Objective To observe the effect of hypoxia on the expression of epithelial growth factor receptor (EGFR) and cell apoptosis of breast and cervical cancer xenografts in nude mouse models.Methods The nude mouse models with MCF-7 and HeLa xenografts were established.The degree of hypoxia and EGFR expression were observed by confocal microscopy.The influence of EGFR expression on cell apoptosis under hypoxia was observed by TUNEL assay.Results EGFR expression was either up-regulated or down-regulated in the MCF-7 and HeLa cells with high degree of hypoxia.Furthermore,the degree of apoptosis was reduced in tumor tissues with high EGFR expression compared with that in those with low expression of EGFR.Conclusion The hypoxia in MCF-7 and HeLa cells exerts heterogeneous effect on EGFR expression.Under hypoxic conditions,EGFR exoression is negatively correlated with cell apoptosis.

Anti-cancer by baicalein combined with U0126 on human breast cancer in vitro / 中国免疫学杂志

Objective:To investigate the effects and mechanisms of anti-cancer by bacailein combined with U0126 on human breast cancer in vitro. Methods: The human breast cancer cell line MCF-7 was treated by baicalein,U0126 and baicalein combined with U0126 respectively. CCK8 assay measured cell proliferation of MCF-7;flow cytometry tested the cell cycle and apoptosis of MCF-7;microscopy observed the amount;TUNEL assay evaluated the apoptosis of MCF-7;Western blot detected the protein level of proliferation and apoptosis related protein;scratch assay measured the ability of migration. Results: Human breast cancer cell line MCF-7 was treated by baicalein or U0126 at different concentration for 24 h, CCK8 assay suggested that both of them can dramatically inhibit MCF-7 proliferation in a dose-dependent way (P<0. 05). Compared to the blank and DMSO groups,the human breast cancer cell line MCF-7 was treated with baicalein for 24 h,the cellular rate at G0-G1 phase increased a lot (91%) (P<0. 05),while the cellular rate at S phase reduced dramatically (P<0. 05),cell apoptosis increased dramatically by microscopy and TUNEL assay(P<0. 05),the level of ERK1/2,CyclinD1 and JNK reduced quickly (P<0. 05). Compared to the baicalein group,MCF-7 was treated by baicalein combined with U0126,the cellular rate at S phase decreased remarkably (P<0. 05),apoptosis was much obvious (P<0. 05),the phosphorylation level of ERK1/2 and JNK reduced a lot (P<0. 05),and the proliferation accelerator CyclinD1 highly decreased (P<0. 05);the scratch assay demonstrated that cell migration was dramatically inhibited when MCF-7 was treated by 20 μmol/L baicalein ( P<0. 05 ) . Conclusion:Both of baicalein and U0126 can inhibit the proliferation and migration,induce the apoptosis of human breast cancer cell line MCF-7 through decreasing the level of ERK, JNK and CyclinD1. Baicalein and U0126 can provide some novel avenues to treat breast cancer in clinic.

Expression and location of TLR5 and NLRC4 in different breast cancer cell lines / 中国免疫学杂志

Objective:To explore the expression and location of TLR5 and NLRC4 on different breast cancer cell lines MDA-MB-231,MCF-7 and MDA-MB-435 and TLR5 activation in breast cancer cell line by recombinant flagellin . Methods:The mRNA level of TLR5 and NLRC4 in MDA-MB-231, MCF-7 and MDA-MB-435 cell were detected with quantitative Real-time PCR and TLR5 expression and location in MDA-MB-231 and MCF-7 cell were detected with Flow cytometry. Induction,expression,purification and i-dentification of recombiant flagellin,including FliC (activating both TLR5 and NLRC4),FliC△90-97(unable to activate TLR5),FliC-L3A (unable to activate NLRC4),FliC△90-97:L3A (unable to activate both TLR5 and NLRC4). 1 μg/ml recombinant flagellin were used to stimulate MCF-7 cell lines,12 h later,the supernate were collected,and ELISA was performed to assess the secretion of IL-8. Results:The mRNA level of TLR5 in MCF-7 cell was 1 700 folds higher than that of MDA-MB-435. TLR5 was expressed in MCF-7 cell surface and ctyosol,while expressed only in cytosol in MDA-MB-231 cell. FliC and FliC-L3A,which were able to activate TLR5 pathway,stimualted MCF-7 cell line to secret IL-8,but FliC△90-97 and FliC△90-97:L3A did not. Conclusion:TLR5 and NLRC4 have been expressed in different breast cancer lines,but there exists difference on the expression level and location of TLR5. Expression level of TLR5 and NLRC4 in MCF-7 cell were higher than other breast cancer lines. TLR5 receptor which is expressed on the surface of breast cancer cell can be activated by flagellin,and these work also provide us experimental basis to further understand the impact of TLR5 activation on breast cancer cell proliferation.

Establishment of drug-resistant cell lines of human triple negative breast cancer and study on their characteristics / 国际检验医学杂志

Objective To establish docetaxel (Doc) resistant MDA‐MB‐231/Doc model and epirubicin (Epi) resistant MDA‐MB‐231/Epi mode from triple negative breast cancer cell line MDA‐MB‐231 and to explore their biological characteristics .Methods The MDA‐MB‐231/Doc and MDA‐MB‐231/Epi drug‐resistant cell lines were respectively established by gradually increasing Doc or Epi concentrations induction method in 12 months .The biological characteristics of the cell lines were compared by the cell mor‐phological observation ,MTT and flow cytometry ;the real‐time fluorescent quantitative PCR was used to detect multi‐drug resist‐ance gene (MDR1) mRNA expression;the expression of P glycoprotein(P‐gp) ,estrogen receptor (ER) ,progesterone receptor (PR) and human epidermal growth factor receptor 2 (Her‐2) was detected by Western Blot .Results After the 12‐month induction ,the established MDA‐MB‐231/Doc could grow stably in the medium containing 12 nmol/L Doc ,and MDA‐MB‐231/Epi could grow stably in the medium containing 800 nmol/L Epi;in the same drug concentration ,the growth proliferation rate of the drug resistant cell line was significantly higher than that of the parental generation cells ,their drug resistance indexes were 8 .32 times and 64 .93 rimes of parental generation sensitive cells ,moreover which showed the mutual cross drug resistant status .Compared to the parental generation cells ,the cells of stage G1 and G2 in two cell lines were increased and the cells of stage S were decreased ,with the prolon‐gation of drug withdrawal time ,the cell proliferation speed was accelerated .The expression level of MDR1 gene was increased in the two drug‐resistant cell lines ,which were 4 .05 times and 5 .96 times of parental generation cells respectively ,P‐gp protein expression was positive .Compared with the MCF‐7 cell line ,ER ,PR and Her2 expression in the MDA‐MB‐231 cell line was negative and typi‐cal triple negative breast cancer cell line .Conclusion The drug resistance cell lines of MDA‐MB‐231/Doc and MDA‐MB‐231/Epi are successfully established with stable growth and drug resistance .

Inhibitory effect of gold nanoparticles conjugated with interferon gamma and methionine on breast cancer cell line

Objective: To develop a gold nanoparticles complex conjugated with interferon-gamma (IFN-γ) and methionine along with application of hyperthermia using near-infrared laser beams for the treatment of cancer cells. Methods: Gold nanorods (10 nm) were conjugated with IFN-γ and methionine using carbodiimide family and characterized after purification by dialysis bags. Breast cancer cells were cultured and incubated with gold nanorods at different concentrations followed by irradiation with near-infrared laser beam. Samples were then evaluated for their viability in order to determine the effect of treatment and variables by MTT assy. Results: Zetasizer results confirmed the conjugation of gold nanorods with methionine and IFN-γ. The median percentage of cell viability in 0.30 μg/mL concentration of gold nanorods was 82%. The cell viability reached to 85% at the same concentration of gold nanorods, which existed in the assayed complex. The results of MTT assay showed that the 0.60 μg/mL concentration of gold nanoparticles complex was toxic on tumor cells (P < 0.05). After exposure to hyperthermia, the viability of cells at 6 min decreased to 77% in 0.30 μg/mL concentration of gold nanorods complex. Conclusions: The size and concentration of gold nanorods was not cytotoxic. However, their presence during irradiation near-infrared laser increased the number of dead cells during the treatment of cells.

The effect of knockdown A20 expression on the proliferation, apoptosis and migration of MCF-7 cells / 安徽医科大学学报

Objective To study the effect of knockdown A20 expression on the proliferation, apoptosis and migra-tion of MCF-7 cells and to evaluate the potential value of the A20 gene as the therapeutic target of breast cancer. Methods Synthesized siRNA targeted to A20 gene or negative control siRNA were transfected into MCF-7 cells by using lipofectamine 2000. CCK8 assay, Annexin V and 7-AAD double staining cytometry, Transwell assay were performed to investigate the effect of knockdown A20 mRNA expression on the proliferation, apoptosis, migration of MCF-7 cells, respectively. Results It can inhibit the proliferation and migration as well as promote the apoptosis in MCF-7 cells by knockdown A20 mRNA expression. Conclusion A20 gene plays an important role in the prolif-eration, apoptosis and migration of MCF-7 cells and it could be a potential therapeutic target of breast cancer.

Role of miR-124 in breast cancer and its underlying mechanism / 中国肿瘤临床

Objective:To evaluate the role of miR-124 in breast cancer and its underlying mechanism. Methods:Quantitative re-verse transcription-polymerase chain reaction (qRT-PCR) was employed to quantify the expression level of miR-124 in the breast can-cer cell lines and matched tissues of 52 patients. Cell proliferation, invasion, and migration of MDA-MB-231 and T-47D were deter-mined by miR-124 overexpression in vitro. Luciferase vectors (pMIR-SP1 3'UTR) were also constructed. The predicted target gene of miR-124 was identified via luciferase activation assay. The mRNA and protein expression of SP1 was detected via qRT-PCR and West-ern blot, respectively. Results:MiR-124 was decreased in breast cancer tissues and cell lines. This result is correlated with metastatic capacity, TMN stages, and prognosis in breast cancer tissues. In breast cancer cell lines, ectopic overexpression of miR-124 inhibited cell proliferation, invasion, and migration in vitro. MiR-124 mimics significantly inhibited luciferase activation (P<0.05) in HEK293 cells and could significantly decrease the mRNA (P<0.05) and protein expression levels of SP1 in MDA-MB-231 and T-47D cells. Con-clusion:MiR-124 could be inhibited in breast cancer. The low miR-124 expression is associated with poor prognosis. In addition, miR-124 could inhibit cell proliferation, invasion, and migration by targeting SP1. These findings confirm that miR-124 downregulation may be a key mechanism for breast cancer carcinogenesis.

Cytotoxicity study of ethanol extract of the stem bark of asam kandis (Garcinia cowa Roxb.) on T47D breast cancer cell line

Objective: To investigate the cytotoxic effect of ethanol extract of the stem bark of asam kandis [Garcinia cowa Roxb. (G. cowa)] on T47D breast cancer cell line. Methods: The cytotoxicity of ethanol extract was carried out against human breast cancer cell line (T47D) by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide colorimetric assay. The extract was added at various concentrations (0.1, 1, 10 and 100 μg/mL). The level of cytotoxicity was determined by calculating the level of IC

Oxidative stress is involved in the apoptosis of human breast cancer MCF-7/ADR cells induced by valdecoxib / 中国药学杂志

OBJECTIVE: To study the effect of selective COX (cyclooxygenase)-2 inhibitor valdecoxib on the growth of human breast cancer MCF-7/ADR(MCF-7/adriamycin) cells. METHODS: MTT assay was used to observe the effect of drugs on the growth of cells. Flow cytometry and Hoechst 33258 dye were used to detect apoptosis of MCF-7/ADR cells. The levels of GSH and GSSG were detected by kit; Laser confocal microscopy was used to detect the levels of ROS. RESULTS: Valdecoxib significantly inhibited the growth of human breast cancer MCF-7/ADR cells and induced apoptosis of the cells. Caspase 3 inhibitor Ac-DEVD-CHO and caspase inhibitor Z-VAD-FMK antagonized the inhibitory effect of valdecoxib on MCF-7/ADR cell growth. Valdecoxib significantly decreased GSH/GSSG ratio and increased the level of ROS, and antioxidant V-acetylcysteine antagonized the inhibitory effect of valdecoxib on MCF-7/ADR cell growth. CONCLUSION: The apoptosis of human breast cancer MCF-7/ADR cells induced by valdecoxib is associated with increase of ROS.

Cellular Effect of Curcumin and Citral Combination on Breast Cancer Cells: Induction of Apoptosis and Cell Cycle Arrest / 한국유방암학회지

PURPOSE: The unmanageable side effects caused by current chemotherapy regimens to treat cancer are an unresolved problem. Although many phytonutrients are useful as chemoprevention without side effects, their effects are slower and smaller than conventional chemotherapy. In the present work, we examined the cumulative effect of two phytonutrients, curcumin and citral, on breast cancer cell lines and compared their effect with the known chemotherapy regimen of cyclophosphamide, methotrexate, and 5-fluorouracil. METHODS: Using cultured breast cancer and normal epithelial cells, the cytotoxic and apoptotic effect of curcumin and citral was evaluated in vitro. The synergistic effect of curcumin and citral was calculated by a combination index study using the method by Chou and Talalay. Cell death pathways and mechanisms were analyzed by measuring intracellular reactive oxygen species (ROS) and apoptotic protein levels. RESULTS: Curcumin and citral caused dose and time dependent cell death and showed a synergistic effect at effective concentration EC50 and above concentrations in breast cancer cells without disturbing normal breast epithelial cells. With combination curcumin and citral treatment, apoptosis induction and cell cycle arrest at G0/G1 phase in breast cancer cells were observed. Curcumin and citral generated ROS and activated p53 and poly (ADP-ribose) polymerase-1 mediated apoptotic pathways. CONCLUSION: The results of this study suggest that curcumin and citral in combination may be a useful therapeutic intervention for breast cancer.

Effect of JNJ-7706621 on cell cycle and apoptosis of breast cancer cell lines / 中国肿瘤临床

Objective:This study aimed to investigate the effects and the molecular mechanism of JNJ-7706621 on cell cycle and apoptosis of breast cancer cell lines. Methods:Breast cancer cell lines T47D and MDA-MB-231 were cultured in vitro and treated with JNJ-7706621 at varying concentrations. MTT assay was used to measure cell proliferation. Flow cytometry was applied to analyze the distribution of cell cycle and apoptotic rates. Western blot was performed to analyze the expression of cyclin B1-CDK, the phosphoryla-tion levels of CDK1Thr161 and CDK1Tyr15, as well as the expression of p53, Bcl-2, caspase3 and poly(ADP-ribose) polymerase (PARP). Results:JNJ-7706621 inhibited the proliferation of the T47D and MDA-MB-231 cells in a dose-and time-dependent manner. Flow cytometry showed that the T47D and the MDA-MB-231 cells in the G2/M-phase significantly increased after treatment at varying concentrations (0, 1, 2, 4μM) of JNJ-7706621:the G2/M-phase rates at the corresponding concentrations were (12.66±1.55)%, (20.63± 1.32)%, (23.20±1.82)%, and (32.19±2.37)%, respectively, for the T47D cells (P<0.05), and the G2/M-phase rates were (16.22±1.48)%, (21.45±0.85)%, (25.25±1.26)%, and (31.08±1.16)%, respectively, for the MDA-MB-231 cells (P<0.05). The rates of apoptotic cells were also significantly increased (P<0.05). Western blot results indicated that JNJ-7706621 exerted a slight effect on the expression of CDK1 and p53 and that the phosphorylation level of CDK1 decreased at the Thr161 site but increased at the Tyr15 site. In addition, cleaved caspase3 and PARP increased, whereas Bcl-2 and cyclinB1 decreased significantly. Conclusion:JNJ-7706621 can significantly inhibit the proliferation of breast cancer cell lines T47D and MDA-MB-231 by inducing cell cycle arrest and apoptosis, which may be associated with the downregulation of the CDK1 phosphorylation at the Thr161 site.

Enhancement of Y14 and Upf1 expression in human breast cancer cell lines / 基础医学与临床

Objective To study expression enhancement and significance of Y14 and Upf1 in human breast cancer cell lines and tissue. Methods Immuocytochemistry and laser scanning confocal microscope(LSCM) were applied. Y14 and Upf1 were determined in human breast cancer cell lines(MCF-7,ZR-75-30,T47D,MDA-MB435s,MDA-MB-453, MDA-MB-231) and breast epithelial cell line ( HBL-100). Results (1) Y14 and Upf1 level of breast cancer cells are obviously higher than that in breast epithelial cell line (P < 0. 05 ). (2)Y14 and Upf1 level of MDA-MB-231 are obviously higher than that in MCF-7. (3)The expression enhancement of Y14 and Upf1 level are obviously higher in human breast cancer tissue. Conclusion The expression level of Y14 and Upf1 in breast cancer cells and tissue enhance obviously.

Chemotherapy sensitivity and associated gene expression in human breast cancer cells / 基础医学与临床

Objective To explore the relationship of chemotherapy sensitivity and expression of multidrug resistance genes and apoptosis regulation genes in human breast cancer cell lines.Methods MTT assay was used to detect the sensitivity to adriamycin(ADM),cisplatinum(DDP),mitomycin C(MMC),fluorouracilum(5-Fu),carmustine(BCNU) in five breast cancer cell lines including Bcap37,MCF-7,T47D,MDA-MB-231and MDA-MB-435.Multidrug resistance genes including P-glycoprotein(P-GP),Glutsthione-s-transferases-?(GST-?),Lung resistance protein(LRP),multidrug resistance related protein(MRP),MGMT and apoptosis regulation genes FAS,BCL-2,P53 and P16 were examined by flow cytometry(FCM).Results The chemotherapy sensitivity was obviously divergent in different breast cancer cell lines.The correlation analysis showed that there were positive correlations between the sensitivity to 5-Fu in breast cancer cell lines and the expression of P16.There was no correlation among the sensitivity to other drugs and expression of other genes.Conclusions The sensitivity to 5-Fu is related to the expression of P16 in breast cancer cell lines.

Effects of triiodothyronine on estrogen receptor-? and thyroid hormone receptor-? in breast cancer cells / 中国癌症杂志

Background and purpose:The effects of triiodothyronine(T3)on breast cancer remain unclear.The aim of this study was to investigate the expression and correlation of estrogen receptor-?(ER-?)and thyroid hormone receptor-?(TR-?)in breast cancer cell lines,and to determine the changes of relevant receptors expression and its possible mechanism due to T3 treatment.Methods:Real-Time PCR was used to analyze the expressions of ER-? and TR-? at mRNA level in seven breast cancer cell lines.The expression level of retinoid X receptor-?(RXR-?)and these two receptors after T3 treatment were determined as well.The gene profile was further determined in SK-BR-3 cells treated with T3.Results:The expressions of ER-? and TR-? were quite low in SK-BR-3,MDA-MB-231 and MDA-MB-435 cells,but high in MCF7,BT20,BT474 and T47D cells.ER-?,TR-? and RXR-? were upregulated due to T3 treatment in ER-?(-)cells,but not in ER-?(+)cells.In SK-BR-3 cells,T3 treatment led to up-regulation of E2F1,TGF-?1R,TGF-?2R and hTERT,but down-regulation of TGF-?1 and p21.Conclusions:The expressions of ER-? and TR-? are correlated in breast cancer cells;the effect of T3 treatment on hormone receptors is associated with endogenous ER-? level.

Enhancement of Y14 and Upf1 expression in human breast cancer cell lines / 基础医学与临床

Objective To study expression enhancement and significance of Y14 and Upf1 in human breast cancer cell lines and tissue.Methods Immuocytochemistry and laser scanning confocal microscope(LSCM) were applied. Y14 and Upf1 were determined in human breast cancer cell lines(MCF-7,ZR-75-30,T47D,MDA-MB-435s,MDA-MB-453,MDA-MB-231)and breast epithelial cell line(HBL-100).Results (1)Y14 and Upf1 level of breast cancer cells are obviously higher than that in breast epithelial cell line(P

Synergistic Cytotoxic Effects of Zole-dronic Acid and Radiation in the MCF-7 Human Breast Cancer Cell Line / 한국유방암학회지

PURPOSE: The clinical use of the zoledronic acid has been increasing recently, and especially for the treatment of bone metastases. The synergistic effects of zoledronic acid with other chemotherapeutic agents have been shown. However it is not known whether a similar synergistic apoptotic effects exist for a combination therapy of zoledronic acid with radiation. METHODS: The MCF-7 human breast cancer cell lines were treated with 10 micrometer, 50 micrometer or 100 micrometer of zoledronic acid, irradiated with 5 Gy, and they were also treated with a combination of both treatments. The results of the synergistic effect on apoptosis were identified by performing XTT assay, DNA fragmentation assay, FACS analysis and western blot analysis at 24, 48, 72 hours after treatment. RESULTS: Zoledronic acid afftects anti-proliferative and apoptotic effects on MCF-7 breast cancer cell line in a dose-dependent manner. The synergistic cytotoxic effect of zoledronic acid and radiation was noted. The western blot analysis suggested that this synergistic effect has a relationship with the intracellular signal pathway especially with Ras, eventhough Bcl-2 and BAX expressions showed no difference in a zoledronic acid and combination treatment group compared to a control group significantly, CONCLUSION: The combined use of zoledronic acid and radiotherapy shows enhanced in vitro cytotoxicity for the MCF-7 human breast cancer cell line. And in vivo study is under way to elucidate the effect of this combination therapy.

STUDY ON THE MECHANISMS OF GENISTEIN AFFECTING THE CHEMOSENSITIVITY OF HUMAN BREAST CANCER CELL LINE MDA-MB-453 TO PACLITAXEL IN VITRO / 营养学报

Objective:To investigate the mechanisms of genistein (GEN) affecting the chemosen- sitivity of human breast cancer cell line MDA-MB-453 to paclitaxel (PTX) in vitro. Method:HER2/neu- overexpressing breast cancer cells MDA-MB-453 were treated by GEN, PTX alone or combined in vitro. Cell cycle was measured by flow cytometry. The expression of HER2/neu protein was observed by immunocytochemistry and. Akt, p-Akt, cyclin B1 and CDK1 protein by Western blot. Results:Cell cycle of MDA-MB-453 cells was blocked at G1/S after treatment of GEN, while at G2/M after treatment with PTX alone. Both GEN and PTX did not change the expression of HER2/neu, total Akt and CDK1 in MDA-MB-453 cells, but GEN significantly decreased p-Akt and cyclin B1 level, and PTX obviously increased cyclinB1 level. GEN antagonized the effects of PTX on level of cyclin B1 protein and blockage of G2/M in MDA-MB-453 cells after treatment with GEN and PTX in combination. Conclusion:The antagonism effects of GEN on the increase of cyclin B1 and blockage of G2/M induced by PTX may be one of the mechanisms of GEN affecting the chemosensitivity of MDA-MB-453 cells to PYX.

Experiment of advancing chemosensitization of Etoposide by insulin in vitro / 中国临床药理学与治疗学

AIM:To investigate the effects of insulin on drug sensitivity of Etoposide(Vp-16) to MBA-MD-543(human breast cancer cell line) in vitro.METHODS:Insulin was applied directly to the MBA-MD-543 cultured in vitro.The effects of insulin and Vp-16 on the number of viable cell,the total number of cells were assayed by MTT method and cell count.RESULTS: Insulin could induce the cell growth and promote the cell metabolism at the concentration(4.0)-(32.0)(mU?ml~(-1))(8-18 hours).At the condition of same density of cells,the administration of insulin((7.5)(mU?ml~(-1))) before adding Vp-16 in 9-15 h,enhanced the chemocytotoxity of Vp-16((70.09)(?g?ml~(-1))) on human breast cancer cells as indicated by MTT colorimetry.CONCLUSION: Proliferation of human breast cancer cell line can be induced by insulin,and insulin can sensitize MBA-MD-543 to the anticancer activity of Vp-16 in vitro. The key of improving the chemotherapeutic effect is the selection of revulsant occasion and concentration.It is possible to increase the growth and metabolism of cancer cells first so as to enhance the chemosensibility,and then administer chemotherapeutic agents,thus improving their theraeutic effects.