High specificity is a key parameter for copper ligands as future therapeutic agents for Alzheimer’s, Wilson’s, and cancer diseases

Objective To investigate the effects of eicosapentaenoic acid (EPA) or EPA plus carboplatin on the proliferation and apoptosis of human lung cancer cell line A-549.Methods A-549 cells were cultured by 100 μg/ml carboplatin,80 μg/ml EPA,and their combination for 48 hours.MTT assay was used to determine the effect of EPA,carboplatin,or their combination on the proliferation of human lung cancer cell line A-549.The morphological changes of human lung cancer cell line A-549 were observed using HE staining,and apoptosis of A-549 cells was analyzed by flow cytometry.Results MTT assay showed that the proliferation inhibition rate of A-549 cells cultured with EPA plus carboplatin was 85.20％ ± 5.00％,which was significantly higher than that of cells cultured with 80 μg/ml EPA (32.85％ ± 3.00％,P =0.0001 ) or 100 μg/ml carboplatin (53.25％ ±3.00％,P =0.0013 ).HE staining showed apoptosis in all three groups,whereas the apoptosis rate reached 17.05％ ± 4.00％ in the combination group,which was significantly higher than that in carboplatin group (9.49％ ± 1.00％,P =0.0252).Conclusion EPA may enhance the effects of carboplatin in inhibiting the proliferation and promoting the apoptosis of human lung cancer cell line A-549. Key words: Eicosapentaenoic acid; A-549 cell lines; apoptosis

Objective To evaluate the role of opioid receptors in fentanyl-induced inhibition of proliferation and migration of human gastric cancer cell line MGC-803.Methods The human gastric cancer cell line MGC-803 was cultured in DMEM liquid culture medium.The cells were seeded in 6-well or 96-well plates and then randomly divided into 4 groups (n =54 each):control group (group C),fentanyl group (group F),naloxon group (group N) and naloxon + fentanyl group (group NF).The cells were exposed to 0.1 μmol/L fentanyl and 10 μmol/L naloxon in F and N groups,respectively.The cells were incubated with 10 μmnol/L naloxon for 30 min and then O.1 μmol/L fentanyl was added to the culture medium in group NF.The viability of the cells was detected by MTT assay after being incubated with fentanyl for 12,24,36,48,60 and 72 h.The cell apoptosis was assessed by flow cytometry after being incubated with fentanyl for 24 h.The migration of the cells was detected by wound healing assay after being incubated with fentanyl for 48 h.The proliferation of the cells was determined by colony formation assay at 7 day of incubation with fentanyl.Results Compared with group C,no significant changes in the viability of the cells,rate of colony formation,apoptotic rate and rate of cell wound healing were found in group N (P ＞ 0.05),and the viability of the cells,rate of colony formation and rate of cell wound healing were significantly decreased,and the apoptotic rate was increased in F and NF groups (P ＜ 0.05).There was no significant difference in the viability of the cells,rate of colony formation,rate of cell wound healing and apoptotic rate between group NF and group F (P ＞ 0.05).Conclusion Opioid receptors are not involved in fentanyl-induced inhibition of proliferation and migration of human gastric cancer cell line MGC-803 in vitro. Key words: Receptors, opioid; Fentanyl; Stomach neoplasms; Neoplasm metastasis

Objective To observe the effect of Kudiezi injection (KDI)on proliferation and apoptosis of human lung cancer cell line A549.Methods After administration of 12.5-400.0 g/L KDI for 24-72 h,the methyl thiazol tetrazolium (MTT) method was used to investigate the inhibitory effect of KDI on A549 cells.Cell apoptosis and cell cycle arrest were investigated by flow cytometry (FCM).Western blot was used to detect the expression of p53 protein.Results KDI significantly inhibit the growth of A549 cancer cells in dose-dependent manners.The number of G0/G1 stage cell was (75.15 ± 1.00)％,(77.52± 1.09) ％,( 79.70 t 1.48 ) ％ and ( 74.55 ± 0.91 ) ％,significant higher than constrol group ( 66.28 ±1.91 )％ (P ＜0.01 ),and that of p53 expression of A549 cancer cells was higher than it in constrol group (P ＜0.05).Conclusion These findings suggest that KDI can inhibit the proliferation of human lung cancer cell line A549 and have obvious dose-effect relationship.The drug inducing people A549 lung cancer cell apoptosis may be relevant to promoting p53 protein expression and its block cells from G1 to S period. Key words: Lung cancer; Kudiezi injection; Proliferation; Apoptosis; Cell cycle; p53

Objective To evaluate the effect of propofol on proliferation of human liver cancer cell line HepG2.Methods HepG2 cells were seeded in 96-well plates (100μl/hole) with a density of 1 × 105/ml and randomly divided into 5 groups (n =33 each)∶ control group (group C),group intralipid (group Ⅰ),and propofol 30,60 and 120μg/ml groups (groups P1-3).In groups P1-3,propofol 30,60 and 120 μg/ml were added to the culture medium and then the cells were cultured for 72 h.In group Ⅰ,10％ intralipid was added to the culture medium and then the cells were cultured for 72 h.The morphology of cells was observed with the light microscope after 24 h of incubation with propofol.The proliferation of the cells was determined at 0,24,48 and 72 h of incubation with propofol.The expression of Fas was determined at 48 h of incubation with propofol.Results The number of the cells was gradually smaller in groups P1-3.The proliferation of the cells was significantly higher in group Ⅰ,while lower in groups P1-3 than in group C (P ＜ 0.05).There was no significant difference in the expression of Fas between group Ⅰ and group C (P ＞ 0.05).The expression of Fas was significantly higher in groups P1-3 than in group C (P ＜ 0.05).The proliferation of the cells was significantly lower,and the expression of Fas was significantly higher in group P3 than in group P1 or group P2 (P ＜ 0.05).Conclusion Propofol can inhibit the proliferation of human liver cancer cell line HepG2 in a concentration-dependent manner and up-regulation of the expression of Fas is involved in the mechanism. Key words: Propofol; Cell line, tumor; Cell proliferation

To explore the effects of icotinib on the proliferation and apoptosis of various lung cancer cell lines. Human lung cancer cell lines HCC827, H1650, H1975, A549 and human epidermal cancer cell line A431 were treated in vitro with icotinib or gefitinib at a concentration gradient of 0 - 40 µmol/L. Their proliferation effects were analyzed by the thiazolyl blue (MTT) assay and the apoptotic effects detected by flow cytometer. The downstream signaling proteins were detected by Western blot. The median inhibitory concentrations (IC(50)) of icotinib for A431 and HCC827 cell lines were (0.04 ± 0.02) and (0.15 ± 0.06) µmol/L respectively. No significant differences existed between the inhibitions of gefitinib and icotinib on A431, HCC827, H1650, H1975 and A549 cell lines (all P > 0.05). Compared with H1650, H1975 and A549 cell lines, icotinib significantly inhibited A431 (P = 0.009, 0.005 and 0.000) and HCC827 (P = 0.001, 0.001 and 0.000) cell lines. And it lowered the expressions of p-AKT, p-ERK and survivin protein expression through the inhibited activity of p-EGFR protein. Icotinib can arrest the proliferation of lung adenocarcinoma cells with EGFR mutation or over-expression by inhibiting the signal pathways of AKT-ERK and survivin.

The widespread consumption of diets rich in anthocyanin and catechin content prompted the evaluation of their in vitro inhibitory effects on cyclooxygenase (COX) enzymes and on the proliferation of human cancer cell lines. Five anthocyanidins consisting of cyanidin (1), delphinidin (2), pelargonidin (3), peonidin (4), and malvidin (5) were tested for COX-1 and -2 enzyme inhibitory activities at 40 μM. Eleven catechins consisting of (+)-catechin (6), (−)-catechin (7), (±)-catechin (8), (+)-epicatechin (9), (−)-epicatechin (10), (−)-epigallocatechin (11), (−)-gallocatechin (12), (−)-epicatechin gallate (13), (−)-catechin gallate (14), (−)-epigallocatechin gallate (15), and (−)-gallocatechin gallate (16) were tested for inhibitory effects of COX-1 and -2 enzymes at 80 μM. Of the compounds tested, the galloyl derivatives of the catechins 11-15, cyanidin (1) and malvidin (5), showed the best COX inhibitory activities compared with the commercial anti-inflammatory drugs ibuprofen (at 10μM), naproxen (at 10 μM), Vioxx® (at 1.67 ppm), and Celebrex(tm)(at 1.67 ppm). Inhibition of the proliferation of the human cancer cell lines MCF-7 (breast), SF-268 (central nervous system, CNS), HCT-116 (colon), and NCI-H460 (lung) was evaluated at concentrations between 100 and 6.25 μM compared with the commercial standard, adriamycin (doxorubicin) at 6.25 μM. At 100-μM concentrations, anthocyanidins 1-5 and catechins 6-10 did not inhibit proliferation of the four cell lines. At 50-μM concentrations, catechins 12, 15, and 16 showed 95%, 100%, and 97% inhibition of breast cells, respectively. At 50-μMconcentrations 12 and 16 were the most effective catechins against colon cells (85% and 93%, respectively) and lung cells (87% and 67%, respectively). CNS cells were the most sensitive of the test cell lines, and total growth inhibition was obtained with catechins 12 and 16 at 100-μMconcentrations. Overall, only the galloyl derivatives of catechins 11-16 inhibited the proliferation of the cancer cell lines.

Objective To study the effect of Notchl gene overexpression on proliferation and cell cycle of human prostate cancer cell line PC-3. Methods Notchl-ORF plasmid and its blank vector were transfected into PC-3 cells respectively. The expression of Notehl or Ki-67 was detected by real-time quantitative polymerase chain reaction （Real-time PCR） and Western blotting. The cell proliferation and cell cycle were analyzed by 3-（4,5-Dimethyhhiazol-2-yl）-5-（3-carboxymethoxyphenyl）-2-（4-sulfophenyl）-2H-tetrazolium （MTS） assay （20 μl/well） and flow cytometry respectively. Results Compared to negative control （3. 574 ± 0. 368 ） and untransfected group （ 3. 306 ± 0. 278）, Notehl expression in NotcH-ORF group （ 43. 740 ± 6. 438 ） was significantly increased （ P 〈 0. 01 ）. Meanwhile, proliferating cell nuclear antigen （Ki-67） level was decreased： 0. 576 ±0. 063, 1. 012 ±0. 011, and 1. 000 ±0. 007 in Notehl-ORF group, negative control group and untransfected group, respectively （P 〈0. 01 ）. MTS assay revealed that the absorbance value in Notchl-ORF group was significantly reduced at 24, 48 and 72 h （P 〈0. 01 ）. Flow cytometry analysis showed that the proportion of cells in G0/G1 phase in Notchl-ORF group was （64. 013 ± 1. 952） %, significantly higher than in negative control group [ （48. 917 ± 2. 771 ） % ] and blank control group [（51.317±1.907）%] （P〈0.01）. Conclusion Overexpression of Notchl gene in PC-3 cells promoted arrest of G0/G1 phase and suppressed cell proliferation probably by down-regulating Ki-67. Key words: Prostate cancer; Notchl gene; Proliferation; Cell cycle

Objective To explore the effects of Fractalkine (FKN) on the biological functions of human pancreatic cancer cell lines SW-1990 and PNAC-1.Methods Adenovirus mediated FKN-small interfering RNA (siRNA) was transfected into human pancreatic cancer cell lines SW 1990 and PNAC-1.The differences in proliferation and invasion ability between before and after FKN-siRNA transfection were determined by clone formation assay,MTT assay and cells invasion assay.After FKN-siRNA transfection,the expression of FKN,tumor necrosis factor (TNF)-α and interleukin (IL)-6 at protein and mRNA level in human pancreatic cancer cell were detected by Western blot and reverse transcription-polymerase chain reaction (RT-PCR).The data were analyzed by one way analysis of variance.Results After human pancreatic cancer cell lines SW-1990 and PNAC-1 transfected with FKN-siRNA,the clone numbers (5.27 ％ ± 0.35 ％ and 4.60 ％ ± 0.30％ ) increased compared with those of control group ( 1.97％ ±0.25％ and 1.77％ ± 0.25％ ) and negative FKN-siRNA group (2.10％±0.30％ and 1.97％±0.25％),and the difference was statistically significant (F=113.51,103.86; both P＜0.05).The clone size was also enlarged.After human pancreatic cancer cell lines SW-1990 and PNAC-1 transfected with FKN-siRNA for 48 hours and 72 hours,the MTT test results showed the absorbance value (48 h:1.28±0.07 and 1.19±0.14; 72 h:1.49±0.11 and 1.52±0.16) was higher than that of control group (48 h:0.80±0.03 and 0.74±0.11;72 h:0.89±0.03 and 0.93±0.04) and negative FKN-siRNA group (48 h:0.85±0.02 and 0.76±0.05; 72 h:0.89±0.02 and 1.07±0.09),and the difference was statistically significant (F=83.80,71.99,17.19,23.51; all P＜0.05).The invasion ability assay showed that the invasion ability of FKN-siRNA transfected cells was stronger than that of control group and negative FKN-siRNA group,and the difference was statistically significant (F=37.37,9.08; both P＜0.05).After FKN-siRNA transfection,the expression of FKN at protein and mRNA level in SW-1990 and PNAC-1 cell line decreased (protein:F=118.93 and 88.62,mRNA:F=47.91 and 72.59),at the same time the expression of TNF-α and IL-6 at protein and mRNA level increased (protein:FTNF-α =112.90 and 77.88,FIL-6 =165.27 and 286.49,mRNA:FTNF-α ==47.93 and 45.19,FIL-6 =36.41 and 23.67),and the differences were statistically significant (all P values＜0.05).Conclusion With siRNA technology to silent FKN function,the proliferation and invasion ability of pancreatic cancer cell lines increased,which indicated FKN might inhibit certain biological functions of pancreatic cancer cells. Key words: Chemokine CX3CL1; Transfection; Pancreatic neoplasms; Cell line,tumor; RNA,small interfering

nm23-H1 gene is a well-known tumor metastasis suppression gene. Our previous study has found that transfection of wild type nm23-H1 gene can significantly downregulate the ERK1/2 activity of human high-metastatic large cell lung cancer cell line L9981. The aim of this study is to investigate the influence of nm23-H1 and exogenous ERK1/2 pathway inhibitor U0126 on the extracellular signal-regulated kinase (ERK1/2) of human high-metastatic large cell lung cancer cell line L9981 and its malignant biological behaviors. The expressive levels of total-ERK1/2, dually phosphorylated ERK1/2 and ERK1/2 relative activity of the human high-metastatic large cell lung cancer cell lines, L9981 (parent cell line with nm23-H1 gene hetero-deletion), L9981-nm23-H1 (transfected with nm23-H1 gene ) and L9981-PLXSN (transfected with vector) were detected by Western blot and immunoprecipitation technique after treating with U0126 (40μmol/L for 20 minutes). The in vitro proliferative and invasive abilities among the above three lung cancer cell lines were determined by MTT and improved Boyden chamber methods. The phosphorylated ERK1/2 expression level and relative activity in L9981-nm23-H1 lung cancer cell line were remarkably lower than those in L9981 and L9981-PLXSN lung cancer cell lines after being treated with U0126 (P < 0.01), but there was no significant difference between L9981 and L9981-PLXSN lung cancer cell lines. No significant difference of total ERK1/2 expression level was observed among the three lung cancer cell lines (P > 0.05) after being treated with U0126. The in vitro proliferation and invasion of L9981-nm-23H1 lung cancer cell line were remarkably lower than those of L9981 and L9981-PLXSN lung cancer cell lines (P < 0.01 ), but no significant difference was found between L9981 and L9981-PLXSN lung cancer cell lines (P > 0.05 ); U0126 could significantly down-regulate the in vitro proliferation and invasion of L9981 lung cancer cell line (P < 0.01). Blocking the activity of ERK1/2 in L9981 lung cancer cell line and transfecting the nm23-H1 gene into the L9981 lung cancer cell line may produce similar cell biological behavior changes, namely the significant reduction of in vitro proliferation and invasion of L9981 lung cancer cell line. These results indicate that the molecular mechanism which nm23-H1 gene reverses invasion and proliferation of the human high-metastatic large cell lung cancer cell line may be related to its effects of down-regulating the activity of the key kinase ERK1/2 of Ras-to-MAPK signal transduction pathway.

Objective To investigate the effects of SAM level on proliferation of human liver cancer cell line HepG2 under the treatment of hepatocyte growth factor (HGF).Methods We established cell systems of different levels of SAM by transfecting pGCSIL-GFP-MAT2A siRNA plasmids into HepG2 cells or adding C3-Ado.The cell system was tested by RP-HPLC.The cell growth curve was drawn by methylthiazol tetrazolium (MTT) assay.Flow cytometry (FCM) was adopted to analyze cell cycle and apoptosis.Results After pGCSIL-GFP-MAT2AsiRNA was transfected successfully,the SAM level was increased to ( 1.35 ± 0.06 ) nmol/mg protein.MTT assay revealed that SAM could suppress the growth of HepG2 cells.Floy cytometry showed that the number of cells in G0/G1 phase was increased by 23.42% and that in G2/M phase decreased by 40.61%,and HepG2 cell apoptosis rate was 34.58%; After C3-Ado being added,the SAM level in HepG2 cells was decreased to (0.37 ± 0.03 ) nmol/mg protein,and proliferation of HepG2 cells was accelerated,the number of cells in G0/G1 phase was decreased by 7.73% and that in G2/M phase was increased by 18.18%,and HepG2 cell apoptosis rate was 5.17%.Conclusion The SAM level in HepG2 cells was the key in the process of HGF promoting proliferation.Only the concentration of SAM was lower level,HGF could promote proliferation of HepG2 cells. Key words: Carcinoma,hepatocellular; siRNA; SAM; Cell proliferation

Objective To investigate the impacts of garcinia acid on the proliferation and invasion abilities of human bladder cancer cell line (BIU-87), and to study the possible molecular mechanisms. Methods The BIU-87 cells were cultured in vitro, and then the cells were divided into control group, low-dose, middle-dose, and high-dose garcinia acid groups. The cells in the drug groups were treated with 20, 40, 80 μmol/L of garcinia acid for 24, 48, and 72 h, and control group were incubated by normal medium. The inhibition of proliferation of BIU-87 cells was performed using CCK8 assay. The abilities of BIU-87 cell invasion were assessed using Transwell chambers, and the expression levels of vascular endothelial growth factor (VEGF) were analyzed using Western Blot technology. Results Compared with control group, the proliferation inhibitory rates of cells after treatment with low-, middle-, and high-dose garcinia acid for 24, 48, and 72 h were significantly decreased (P<0.05). Moreover, the proliferation inhibitory rates in different drug groups were greatly increased with the time extension. Compared with control group, the number of cells passing through the membrane(26 ± 4, 41 ± 4, 53 ± 5 vs. 119 ± 7) in low-, middle-, and high-dose garcinia acid group significantly decreased (P<0.05), the expression levels of VEGF (41.2 ± 6.2, 23.8 ± 5.2, 17.9 ± 4.7 vs. 14.8 ± 4.2) in low-, middle-, and high-dose garcinia acid group significantly decreased (P<0.05). Conclusions The Garcinia acid can inhibit the proliferation and invasion of BIU-87 cells via the down-regulation of VEGF expression. Key words: Cell proliferation; Neoplasm invasiveness; Vascular endothelial growth factors; Garcinia acid

The aim of this study was to assess the possible roles of the phytochemical compounds, curcumin, quercetin and resveratrol in the proliferation of human colorectal cancer cell line Caco-2. All three phytochemical compounds inhibited Caco-2 cell proliferation, with curcumin being more effective than quercetin and resveratrol. Investigations concerning DNA fragmentation in the nucleus, Bax and Bcl-2 mRNA expression levels, and caspase-3/7 activity indicated that curcumin induced apoptosis in Caco-2 cells through an increase in the Bax/Bcl-2 ratio and activation of caspase-3/7. Furthermore, the analysis of flow-cytometry showed that curcumin caused an arrest of G2/M phase in Caco-2 cells. These results suggest that curcumin suppresses Caco-2 proliferation partially via activation of the mitochondrial apoptotic pathway and cell cycle retardation.

An increasing body of evidence implicates obesity and the attendant hyperinsulinemia as major risk factors for human colorectal cancers. The lipogenic pathway supports growth and survival of colon cancer cells. In particular, inhibition of Fatty Acid Synthase (FASN) or Acetyl-CoA Carboxylase α (ACCα) induces apoptosis of colon cancer cells. The relative involvement in colon cancer initiation, progression and pathogenesis of cytosolic NADPH that is used in lipogenesis remains less clear. In the present study, we have determined the effects of insulin and the involvement of the major NADPH-generating cytosolic enzymes on proliferation of human colon cancer cell lines. Insulin (1-10 nM; to mimic normo- to hyper-insulinemic states) induced a significant increase (7-15%, p &amp;lt; 0.05) in proliferation of HT-29 and HCT-116 colon cancer cell lines in vitro (assayed by MTT assay). Addition of insulin augmented (by 5-10%) proliferation of both cell lines upon concurrent treatment with cancer chemotherapeutic agents (5-fluorouracil, oxaliplatin, irinotecan; each added at a dose &amp;lt; EC50). The insulin-mediated increase in HT-29 cell growth was associated with a 2-3 fold elevation in FASN gene expression and a 50% decrease in expression of the FASN-targeting micro RNAs, miR-103 and miR-107. However, insulin did not induce mRNA abundance for the cytoplasmic NADPH-generating enzymes [Malic Enzyme 1 (ME1), Glucose 6-Phosphate Dehydrogenase (G6PD), 6-Phosphogluconate Dehydrogenase (6PGD), or Isocitrate Dehydrogenase-1 (IDH1]. siRNA-mediated knockdown of FASN or of the individual major cytosolic NADPH-generating enzymes caused decreases in proliferation of HT-29 and HCT-116 cells (15-30%, p &amp;lt; 0.05) compared to the control scrambled siRNA. Data highlight pro-proliferative roles for insulin, FASN and cytosolic NADPH-generating enzymes in colorectal cancer cell growth. Implementation of pharmacologic and/or nutritional means to reduce serum insulin levels, enhance FASN miR expression and inhibit tumor cell NADPH-generation may serve as useful adjuncts for future cancer treatment and prevention. Supported by NIH grant RO1 CA136493 and the Arkansas Biosciences Institute. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4072. doi:10.1158/1538-7445.AM2011-4072

Objective To investigate the role of Annexin A9 (ANXA9) in the proliferation of human colon cancer cell line SW620 and the underlying mechanism. Methods The expression of ANXA9 in human colon cancer cell lines HT29, SW620, SW480, LoVo and SW1116 was detected by real-time quantitative polymerase chain reaction (Real-time PCR) and Western blotting. SW620 cell lines with the strongest expression of ANXA9 was transfected with 40 nmol/L ANXA9-small interfering RNA (siRNA) to inhibit the expression of ANXA9. Cell counting kit-8 (CCK-8) assay and flow cytometry (FCM) were correspondingly used to examine the effect of transfection on the activity and cell cycle of SW620 cells. The expression of proliferating cell nuclear antigen (PCNA), Cyclin D, Cyclin E, p21 and p16 was detected by Real-time PCR and Western blotting. Results The mRNA and protein expression levels of ANXA9 in SW620 cells were the highest in human colon cancer cell lines HT29, SW620, SW480, LoVo and SW1116 and mRNA expressions were as following: 0.027±0.004, 0.041±0.005, 0.028±0.003, 0.033±0.003, 0.025±0.005; protein expressions were as following: 0.287±0.076, 1.246±0.103, 0.326±0.040, 0.387±0.097, 0.295±0.064 (F=8.212, P=0.003; F=81.728, P=0.000). Expressions of ANXA9 mRNA and protein in transfection group, control group, blank group were (0.209±0.016, 0.317±0.104), (0.957±0.070, 0.647±0.155), (1.031±0.171, 0.727±0.145). The ANXA9 mRNA and protein expression in the transfection group was significantly lower than in the control and blank group (F=54.072, P=0.000; F=7.601, P=0.023). Results of CCK-8 showed that cell activity in transfection group, control group, blank group was as following: 24 h (0.605±0.024, 0.612±0.022, 0.628±0.027), 48 h (0.810±0.049, 1.196±0.118, 1.308±0.070), 72 h (1.145±0.070, 1.531±0.062, 1.454±0.081). Cell activity in transfection group were significantly lower than the control and blank group (F=38.742, P=0.000; F=32.56, P=0.000). The percentage of cells in G0/G1 phase, G2/M phase, S phase was (66.870±3.850)%, (15.060±2.480)%, (18.080±1.420)% in transfection group; 50.070±3.370)%, (32.520±2.500)%, (17.410±0.920)% in control group; (48.740±2.170)%, (32.390±1.820)%, (19.210±0.390)% in blank group. The percentage of G0/G1 phase cells in the transfection group increased (F=29.752, P=0.001), and the proportion of G2/M phase decreased (F=57.860, P=0.000), while the proportion of S phase cells had no significant change (F=1.568, P=0.284). The expression of Cyclin D1 and Cyclin E1 was significantly lower after ANXA9-siRNA transfection (mRNA: F=462.821, 5.512, P=0.000, 0.044; protein: F=15.148, 8.300, P=0.005, 0.019), and that of p21 was significantly increased (mRNA: F=6.742, P=0.032; protein: (F=21.230, P=0.002). Conclusion ANXA9 may participate in the proliferation of colon cancer cell line SW620 possibly through the expression of Cyclin D1, Cyclin E1, p21. Key words: Colon cancer; Annexin A9; Proliferation

A well‐suited model to simulate cellular population dynamics is the two‐dimensional cellular automaton model, which consists of a lattice of sites, the value ai,j of each site being updated in discrete time steps according to an identical deterministic rule depending on a neighbourhood of sites around it. A cellular automaton is described which mimics cell population proliferation by replacing the site values by the age and the cycle phase of cells. The model takes into account the size of the cells. It is used to simulate the proliferation of the human breast cancer cell line MCF‐7 and the results of the simulation are compared with experimental data obtained from a light microscopic image analysis of the proliferation process. The initial configuration of the cellular automaton is obtained from the discretization of the results of the initial stage of the image processing. After each day of proliferation the pattern obtained from the simulation is compared to the experimental result of the corresponding image analysis. The comparison is made from a topographical point of view through the concept of the minimal spanning tree graph. The agreement between experiment and model is a good starting point to complex models such as cell proliferation under growth effectors or drugs.