ABSTRACT
@#Objective: To investigate the expression of lncRNA LINC00886 in human esophageal squamous cell carcinoma (ESCC) tissues and cell lines, and its effects on proliferation, migration and invasion of Eca109 cells. Methods: The cancer tissues and corresponding para-cancerous tissues of 69 ESCC patients were collected in the biological specimen bank of the Fourth Hospital of Hebei Medical University from June 2014 to December 2016; the ESCC cell lines Eca109, TE13, TE1, Kyse150, Yes-2 and Kyse170 were also collected. LINC00886 gene expression in ESCC tissues and cell lines was detected by qPCR. Eca109 cells were transfected with pIRES2-LINC00886 and pIRES2-NC, respectively, and the overexpression efficiency of LINC00886 gene in Eca109 cells was detected by qPCR; MTS, clone formation assay, wound-healing assay and Transwell invasion assay were respectively used to detect the effect of LINC00886 over-expression on proliferation, migration and invasion ability of Eca109 cells. Results: The expression of LINC00886 gene in ESCC tissues was significantly lower than that in para-cancerous tissues (P<0.01), and its expression level was associated with tumor TNM stage and lymph node metastasis (both P<0.05). The expression level of LINC00886 gene in ESCC cell lines was also lower than that of the control group (all P<0.01). Compared with control group, the expression level of LINC00886 gene was significantly higher in Eca109 cells transfected with pIRES2-LINC00886 (both P<0.05). Compared with the control group, LINC00886 overexpression significantly inhibited the proliferation, migration and invasion abilities of Eca109 cells (all P<0.01). Conclusion: The decreased expression of LINC00886 gene may be related to the occurrence and development of ESCC. Over-expression of LINC00886 gene inhibits the proliferation, migration and invasion abilities of ESCC cells.
ABSTRACT
@#Objective: To investigate the expression of lncRNA01296 in esophageal cancer (EC) tissues and its effect on the proliferation and migration of EC TE-2 cells. Methods:Atotal of 36 pairs of esophageal cancer tissues and corresponding para-cancerous tissues were collected from EC patients admitted to the Department of Thoracic Surgery,Affiliated Hospital of Chengde Medical College from January 2017 to September 2018. The human normal esophageal epithelial (HEEC) cells and human esophageal cancer cell lines ECA109, TE-1 and TE-2 were cultured. qPCR was used to detect the mRNAexpressions of lincRNA01296, SNRPA(small nuclear ribonucleoproteinA) and NGF (nerve growth factor) in EC tissues and cells. Recombinant lentiviral interference vectoror control vector were used to transfect EC cell lines, as sh-lncRNA01296#1,#2 and Mock groups. WB was used to detect the protein expressions of SNRPAand NGF in transfected cells. MTS assay was used to detect cell proliferation, and Transwell assays were used to detect cell invasion and migration of TE-2 cells after transfection. Results: The mRNAexpressions of lncRNA01296, SNRPAand NGF were significantly increased in esophageal cancer tissues and cell lines (all P<0.01), and these expressions in poorly differentiated TE-2 cells were higher than those in highly differentiated ECA109 and TE-1 cells (all P<0.05). The mRNAexpressions of lncRNA01296 and NGF in sh-lncRNA01296#1 and sh-lncRNA01296#2 groups were significantly lower than those in Mock group (all P<0.01), while the mRNAexpression of SNRPAshowed no statistical difference among three groups (P>0.05). The protein expressions of lncRNA01296 and NGF in sh-lncRNA01296#1 and sh-lncRNA01296#2 groups were significantly lower than those in Mock group (all P<0.01). The relative proliferation ability of cells in sh-lncRNA01296#1 and shlncRNA01296#2 groups was significantly lower than that of Mock group at 48 and 72 h after transfection (P<0.05 or P<0.01). The number of invasive cells was (72.0±6.3), (36.6±4.3) and (33.9±3.7) in Mock, sh-lncRNA01296#1 and sh-lncRNA01296#2 groups, respectively; and the number of migrated cells was (85.2±9.9), (47.5±8.1) and (43.8±6.5), respectively, indicating that the numbers of invasive and migrated cells in sh-lncRNA01296#1 and sh-lncRNA01296#2 groups were significantly less than those in Mock group(all P<0.01). Conclusion: lncRNA01296 can up-regulate SNRPAexpression to promote NGF-mediated proliferation and metastasis of EC cells, which may provide new target for the diagnosis and treatment of esophagealcancer.
ABSTRACT
@#Objective: To detect the expression of non-receptor protein tyrosine phosphatase 6 (PTPN6) in different esophageal squamous cell carcinoma (ESCC) cell lines, and to investigate its effect on proliferation, migration and invasion ability of Eca109 and Yes-2 cell lines. Methods: qPCR was applied to detect the mRNA expression of PTPN6 in different ESCC cell lines (TE1, Eca109, Kyse150, Kyse170 and Yes-2). pcDNA3.1-PTPN6 plasmid was transiently transfected into Eca109 and Yes-2 cells respectively. The expression of PTPN6 was detected by real-time PCR and Wb. The effects of PTPN6 over-expression on the biological behaviors of ESCC cells were detected by MTS, colony formation assay, wound healing assay and Transwell assay, respectively. Results: The mRNA expression of PTPN6 was remarkably reduced in ESCC cell lines (TE1, Eca109, Kyse150, Kyse170 and Yes-2) compared to normal esophageal epithelial cells (HEEpiC) (P<0.05). Compared to the mock cells, significant up-regulation of PTPN6 was detected in pcDNA3.1-PTPN6 transfected Eca109 and Yes-2 cells (all P<0.05 or P<0.01); PTPN6 over-expression led to a significant inhibition in migration and invasion ability of Eca109 and Yes-2 cells (all P<0.05). Conclusions: Over-expression of PTPN6 may inhibit the proliferation, migration and invasion of ESCC cells, which might be an important factor influencing the biological characteristics of ESCC cells.
ABSTRACT
@#Objective: To investigate the effects of ezrin enhancer knockout on ezrin gene expression, cell proliferation and migration of human esophageal carcinoma Eca-109 cells. @*@#Methods: The CRISPR/Cas9 recombinant plasmids targeting upstream/downstream of human ezrin enhancer were co-transfected into human esophageal carcinoma Eca-109 cells, and the cell line Eca-C2 with ezrin enhancer knockout was screened by purinomycin. Then the expression levels of ezrin mRNAand protein in Eca-C2 cells were detected by Real-time quantitative PCR (qPCR) and Western blotting, respectively; The expression levels of MAPK-pathway-related proteins were detected by protein array technology; and the effects of ezrin enhancer knockout on the proliferation and migration of Eca-C2 cells were analyzed by WST-1 method and wound-healing assay, respectively. @*@# Results:The human esophageal carcinoma cell line Eca-C2 with stable ezrin enhancer knockout was established successfully. Compared with control cells, the mRNA and protein expressions of ezrin in Eca-C2 cells were significantly reduced (all P<0.05).Among the 17 detected MAPK pathway related proteins in Eca-C2 cells, 9 proteins (AKT, CREB, GSK3b, MKK6, mTOR, P38, P53, P70S6K and RSK1) were down-regulated, and the cell proliferation and migration were significantly inhibited (all P<0.05).@*@# Conclusion: ezrin enhancer knockout can significantly inhibit the cell proliferation and migration of human esophageal carcinoma Eca-109 cells.
ABSTRACT
@# Objective: To investigate the expression of long non-coding RNA NUP50-AS1 (lncRNA NUP50-AS1) in esophageal squamous cell carcinomas (ESCC) tissues and cell lines, and to explore its effect on proliferation, migration and invasion of human esophageal cancer Eca109 cells. Methods: 49 pairs of ESCC tissues and corresponding para-cancerous tissues obtained from the Biological Specimen Base of the Fourth Hospital of Hebei Medical University during Jan. 2015 to Jan. 2016 were used in this study. qRT-PCR method was applied to detect the expression of NUP50-AS1 in collected tissues samples and five esophageal cancer cell lines (TE1, TE13, Eca109, Kyse150 and Kyse170). ShRNAs were transiently transfected into Eca109 cells to interfere the expression of NUP50AS1 gene, and finally, sh2-NUP50-AS1 was used for the following experiments. The effect of NUP50-AS1 gene knockdown on the proliferation of Eca109 cells was detected by MTS and colony formation assay; the effect of NUP50-AS1 gene knockdown on the migration of Eca109 cells was detected by scratch test, and the effect on cell invasion was detected by Transwell assay. Results: The expression of NUP50-AS1 in ESCC was correlated with the lymphnode metastasis and TNM stage (all P<0.01). The expression of NUP50AS1 in ESCC tissues was significantly higher than that in corresponding normal tissues (2.003±0.870 vs 1.000±0.000, P<0.05). The expression of NUP50-AS1 in five esophageal cancer cell lines was significantly up-regulated (P<0.05), and it had the highest expression in Eca109 cell line. After transfection, sh2-NUP50-AS1 had the highest transfection efficiency, and knocking down NUP50-AS1 gene significantly inhibited the proliferation, invasion and migration of the Eca109 cells. Conclusion: The expression of lncRNA NUP50AS1 in ESCC tissues was significantly higher than that in the para-cancerous tissues, and correlated with the TNM stage and lymphnode metastasis. The down-regulation of NUP50-AS1 inhibited the proliferation, invasion and migration of esophageal cancer cells. The high expression of NUP50-AS1 gene may be closely related to the occurrence and development of ESCC.
ABSTRACT
Objective To discuss the effect of α-asarone on the expression level of Cyt-c,Smac,Caspase3 mRNA and protein in human esophageal carcinoma Eca-109 cell mitochondria. Methods The Eca-109 cells were cultured in vitro,and divided into the negative control group and the α-asarone treatment groups(final concentration:25,50,100 μg·mL-1).After 48 h,the morphological changes of Eca-109 cells were observed by fluorescence inversion microscope.The total RNA of cells were extracted by TRIzol method,the expressions of Cyt-c、Smac and Caspase3 were measured by RT-PCR and Western blotting. Results After Eca-109 cells were treated with different concentrations of α-asarone for 48 h,and obvious changes in the morphology were observed,the expressions of Cyt-c,Smac and Caspase3 genes and protein were increased significantly compared to the negative control group( P<0.05). Conclusion α-asarone can induce the human Eca-109 cells apoptosis by regulating expressions of mitochondrial apoptosis pathway correlation genes such as Cyt-c,Smac and Caspase3.
ABSTRACT
Objective To investigate the effects of inhibition of MDC1 protein expression on xenografted tumors in nude mice,and to observe the histopathological and cellular changes in nude mice.Methods Three pairs of effective and control short hairpin RNA targeting MDC1 mRNA were designed and cloned into the pSIH1-H1-copGFP vector.Real-time PCR and Western blot were used to determine the mRNA and protein expression of MDC1.After selection by copGFP reporter gene,cells were divided into negative transfection group (ECA109-N) and MDC1 transfection group (ECA109-M).The transfected cells were injected into nude mice.The mice were divided into ECA109 group,ECA109-N group,and ECA109-M group.Each group was divided into irradiation subgroup and non-irradiation subgroup.The changes in tumor size after irradiation were evaluated in each group.Western blot was used to measure the expression of CHK1,CHK2,and CHK2T68 in xenografted tumors.Flow cytometry was used to analyze the cell cycle distribution and apoptosis of tumor cells in nude mice.The variance analysis was used to compare the mean of multiple groups,and the SNK-q test was used in the two two groups.Results The pMDC1-shRNA plasmid was successfully constructed and used to transfect ECA109 cells.ECA109-M cells were obtained by stable transfection with the recombinant plasmid.All inoculated nude mice survived with visible xenografted tumors at the underside of the paw in about one week.There was no swelling and wound in inoculation sites.There was no significant difference in tumor size between different groups (P＞0.05).The tumor growth in the ECA109 group and the ECA109-N group significantly slowed down after irradiation with a dose of 15 Gy (P＜0.05).Compared with the other two groups,the ECA109-M group had a significant smaller tumor size,significantly slower relative tumor growth,and significantly higher growth inhibition (all P＜0.05).The q value of the ECA109-M group was 1.36.In the ECA109-M group,there were no significant changes in the protein expression of CHK1 and CHK2 after irradiation (P＞ 0.05);however,the phosphorylation of CHK2T68 protein was significantly reduced after irradiation (P＜0.05).There were no significant differences in cell cycle distribution or the proportion of apoptotic cells in tumor tissue between the three groups (P＞0.05).Conclusions Inhibition of MDC1 protein expression by RNA interference can effectively inhibit the growth of xenografted tumors after irradiation in the nude mice by increasing their radiosensitivity.
ABSTRACT
Objective To investigate the expression of Nek8 in esophageal squamous cell carcinoma(ESCC) tissues and cell line , and to evaluate its correlation with the clinicopathological features of ESCC and the survival rate of ESCC patients after operation . Methods The expression of Nek8 mRNA in human ESCC Eca109 cell line and two pairs of ESCC tissues and adjacent normal e‐sophageal mucosal epithelium were detected by semi‐quantitative reverse transcription polymerase chain reaction (RT‐PCR) .Immu‐nohistochemistry and tissue microarray technique were used to examine the expression of Nek 8 protein in ESCC tissues and tumor‐adjacent tissues .The correlation between Nek8 expression and clinicopathological features of ESCC and survival rate of ESCC pa‐tients was then analyzed .Results The expression of Nek8 mRNA was positive in Eca109 cells and two cases of ESCC tissue ,and it was negative in paired normal esophageal mucosal epithelium specimens .In tissue microarray ,the expression of Nek8 protein in ES‐CC tissues ,which was mainly in the cytoplasm ,was significantly higher than that in tumor‐adjacent tissues(P= 2 .16E‐13) .The high expression of Nek8 was associated with tumor size (P=0 .008) ,but not with sex ,age ,histological grade ,infiltration degree , lymph node metastasis ,and the survival rate(P>0 .05) .Conclusion The expression of Nek8 is up‐regulated in ESCC tissues and cell line ,and may be involved in tumorigenesis and development of ESCC .Nek8 could act as a potential biomarker for ESCC diag‐nose and target for therapy .
ABSTRACT
Objective:To investigate the effects of epidermal growth factor (EGF)on cell cycle and cell cycle-related regulatory factors of human esophageal squamous cell carcinoma (ESCC) cell line Eca109.Methods: Serum starved Eca109 cells were treated with 20 ng/ml recombinant human EGF(rhEGF)for 24 h.The cell cycle phase distribution was detected by flow cytometry.The mRNA and protein expression levels of p21CIP1/WAF1(p21) and p27KIP1(p27) were detected by real-time quantitative reverse transcription polymerase chain reaction(qRT-PCR)and Western blot,respectively.Results: The proportions of G1 phase cells in EGF group and control group were ( 54.90 ±0.82 )% and ( 65.94 ±0.74 )%.The mRNA and protein expression levels of p 21 in EGF group was significantly higher ,and p27 was significantly lower than that in control group ( P<0.01 ) .Conclusion: EGF facilitates G1-S phase transition,and promotes the proliferation of Eca 109 cells,which may be associated with the up-regulation of p21 and down-regulation of p27.
ABSTRACT
Objective To construct a small interfering RNA (siRNA) vector targeting ΔNp63α and investigate ΔNp63α gene interference on the proliferation and apoptosis of human esophageal squamous carcinoma Eca109 cell line. Methods Adeno-associated virus (AAV)-ΔNp63αshRNA driven by H1 promoter was constructed and was used to infect Eca109 cells. AAV-Null and normal cell lines were utilized in the control group and blank control group, respectively. The influence of siRNA interference of ΔNp6α expression on the growth, proliferation, tumorigenic efficiency and apoptosis of Eca109 cells were analyzed in vitro and in vivo. Results Compared with the two control groups, the specific siRNA targeting ΔNp63α gene significantly down-regulated the expression of ΔNp63α protein levels in Eca109 cells (all P<0.05). The growth of Eca109 cells infected with AAV-ΔNp63αshRNA was significantly lower than those in the two control groups (all P<0.05). Cell cycle analysis showed the proliferation index (PI) of AAV-ΔNp63αshRNA infected cell line was significantly lower compared with the two control groups (all P<0.01). In vivo experiment exhibited that AAV-ΔNp63αshRNA infected cells resulted in a lower tumor weight in nude mice compared with the cells in the two control groups (all P<0.05). In addition, the apoptosis index (AI) of AAV-ΔNp63αshRNA infected cells were significantly higher than those of the other cell lines (P<0.05). Conclusion AAV- mediated expression of shRNA can significantly reduce ΔNp63α expression in Eca109 cells, slowing down the proliferation, promoting the apoptosis, and subsequently inhibiting the growth of tumor.
ABSTRACT
Objective: To study the effect of baohuoside-I extracted from Periplocae Cortex on proliferation and Wnt/β-catenin signaling pathway of human esophageal carcinoma cell Eca-109. Methods: The expressions of β-catenin, Cyclin D1, and Survivin protein in Eca-109 cells were measured with flow cytometry (FCM). The expressions of β-catenin, Cyclin D1, and Survivin mRNA were detected by RT-PCR. Results: After treatment with 25 and 50 μg/mL of baohuoside-I for 48 h, the expression levels of β-catenin, Cyclin D1, Survivin mRNA, and protein were decreased significantly (P<0.01), but with 12.5 μg/ML of baohuoside-I the expression level was not decreased significantly compared with the control group. Conclusion: Baohuoside-I from Periplocae Cortex could inhibit the proliferation of Eca-109 cells. This effect associais with down-regulation expression of β-catenin, Cyclin D1, Survivin, and their proteins, which affects on the Wnt/β-catenin signaling pathway.
ABSTRACT
Objective To study the change of DNA polymerase beta and XRCC1's expression during malignant celI differentiation.Methods The Eca-109 cells were divided inm 2 groups:differentiation group which cultured with 8-Br-cAMP and control group.The 2 groups cells were cultured 48h simultaneously.The immunocytochemistry was performed to detect the expression of DNA polymerase beta and XRCC1.Results Compared with control group,the expression of DNA polymerase beta and XRCC1 was decreased simultaneously(P＜0.05).Conclusion The differentiation agent can down-regulate the expression of DNA polymerase beta and XRCC1,suggesting that overexpressed DNA polymerase beta and XRCC1 maybe result in mutator phenotype.
ABSTRACT
Objective To investigate human esophageal cancer Eca109 cells apoptosis induced by resveratrol.Methods Eca109 cells were treated with difierent concentrations of resveratrol and the change of morphology was observed by inverted microscope and transmission electron microscope in different time;The cell growth inhibitory rate of resveratrol on the proliferation of Eca109 cells were evaluated in vitro by MTT assay.Flow cytometry (FCM)analysis was used to determine the apoptosis of Eca-109 cells.Results Resveratrol was able to inhibit the growth of Eca109 cells,and the suppressive effect was increased with treating concentration and treating time.Resveratrol inhibited the growth of esophageal cancer Eca109 cells in a dose-and time-dependent manner and induced the apoptosis in esophageal cancer.Conclusion Resveratrol could inhibit the proliferation of Eca-109 cells and block the cell cycle at G0/G1.And in the end resveratrol could induce the apoptosis of Eca109 cells.
ABSTRACT
Objective To investigate the effects of 2-(3carboxy-1-oxoprogy1)amino-2-deoxy-D-glucose(COPADG) on the proliferation and cell cycle of human esophageal cancer cells Eca-109 and TE-1.Methods In vitro experiments,MTT colorimetric assay was performed to determine the growth inhibitory rates of Eca-109 and TE-1 cells treated by COPADG.Flow cytometry was applied to observe the change of cell proliferation cycle and apoptosis index.Cell morphological change was observed by transmission electron microscopy.Results COPADG inhibited effectively the growth of esophageal cancer cells Eca-109 and TE-1 in a time-and dose-dependent manner(P
ABSTRACT
Aim To study the effects of selective cyclooxygenase-2 (COX-2) inhibitor,nimesulide,on COX-2 expression, cell proliferation and apoptosis of human esophageal carcinoma Eca-109 cell lines. Methods MTT assay was used to observe the proliferative effect;COX-2 mRNA expression was evaluated with RT-PCR; COX-2 protein expression,cell cycle and apoptosis were analyzed with flow cytometry;microscope and agarose gel electrophoresis of DNA were also used to observe the apoptosis. Results Nimesulide significantly inhibited the proliferation of Eca-109 cell lines in a time and dose-depenent fashion, down-regulated the expression of COX-2 mRNA and COX-2 protein in a dose-dependent fashion;nimesulide also decreased the proliferation index and the proportion of cells in S phase, meanwhile increased the proportion of cells in G_0/G_1 phase and induced apoptosis. Conclusion COX-2 selective inhibitor nimesulide inhibits proliferation,induces apoptosis and cell cycle arrest of human esophageal cells via down-regulation of COX-2 expression.
ABSTRACT
Objective To investigate the in vitro inhibitory effect of LIGHT on human esophageal carcinoma cells. Methods LIGHT Fc expression vector was transfected into human esophageal squamous carcinoma cell line, Eca109. The inhibitory effect of LIGHT gene on cell growth was detected by MTT and cell growth curve. The expressions of LT?R and HVEM were detected by RT PCR. Results Expression of LIGHT Fc gene could inhibit Eca109 cell proliferation. The growth curve of Eca109/LIGHT was significantly lower than that of the control group in the culture medium containing 1% FCS. MTT test showed that there was significant difference in cell viability between Eca109/LIGHT and the control group ( P
ABSTRACT
AIM: To observe the inhibitory effects of polypeptide from Buthus martensii venom (PBMV) on human tumor cell lines and the influence of PBMV on cell cycle migration, expression of tumor-suppressor gene p53 and the membrane potential of CNE-2Z cells. METHODS: MTT colorimetric method, the colony formation and mitosis index, flow cytometry assay and intracellular recording with glass microelectrodes were used. RESULTS: PBMV had obvious cytotoxicity on several tumor cell lines. The cells grow was inhibited by PBMV, colony formation rate and mitotic index of tumor cells were reduced and the number of polykaryocyte was decreased. CNE-2Z cells in S phase were reduced evidently after they were treated with PBMV (P
ABSTRACT
Aim To investigate the effect and mechanism of valdecoxib on the apoptosis of human esophageal cancer cells.Methods Flow cytometry was used to observe the effect of valdecoxib on apoptosis and the cell cycle distribution of Eca109 cells.Transmission electron microscope was further used to detect the cell apoptosis.The content of LDH was examined using LDH kit.The expressions of p-p38MAPK,Fas and FasL protein were detected using flow cytometry.Results Valdecoxib of 25～400 ?mol?L~(-1) significantly induced the apoptosis of Eca109 cell line,and the rate of apoptosis was increased from(2.95?0.83)% to(48.46?0.73)%,50～400 ?mol?L~(-1) valdecoxib also decreased the proliferation index and the proportion of cells in the S phase,increased the proportion of cells in the G_0/G_1 phase,but had no effect on the proportion of cells in the G_2/M phase.Compared with those in Eca109 cells cultured in the medium with solvent,the expression of p-p38MAPK,Fas and FasL was higher in the Eca109 cells exposed to valdecoxib in a dose-dependent manner in 72 h.Conclusion Valdecoxib can induce apoptosis of Eca109 cell line partly by up-regulating the expression of p-p38MAPK/Fas/FasL.
ABSTRACT
Aim To investigate the regulatory effect of p38MAPK signal pathway on the apoptosis of human esophageal cancer cells induced by valdecoxib.Methods The tumor cells were inoculated in the dose of 1?107?L-1.After 6 h,the cells were divided into control group,solution group,400,200,100,50,25 ?mol?L-1 valdecoxib group and various concentration valdecoxib+SB203580 group,cultured for 72 h.FCM and DNA Ladder were used to detect the apoptosis of Eca109 cells.p38 mRNA expression was detected by RT-PCR.The expression of p-p38MAPK protein was detected by immunohistochemical staining and FCM.Results ① Valdecoxib could increased the apoptosis rate of Eca109 cell in concentration-dependent fashion.Apoptosis rate was increased to 48.46% in 400 ?mol?L-1 valdecoxib group at the incubation time of 72 h.DNA ladder was the most recognized marker of apoptosis,and there was obvious DNA ladder in valdecoxib treated group,especially in 400 ?mol?L-1 group.② Valdecoxib could increase the expression of p38MAPK,while SB203580 could inhibit the over-expression induced by valdecoxib,at the same time,the apoptosis rate was been decreased.③ The expression of p38MAPK protein was positively correlated with the apoptotic rate(r=0.822,P=0.000).Conclusions Valdecoxib could activate p38MAPK pathway,thus induce the apoptosis of Eca109 cells,which may be one of the mechanisms for the inhibition of cell growth by valdecoxib.
ABSTRACT
Aim To investigate the inhibitory effect of paeonol (Pae) on the human esophageal cancer cell line Eca-109 in vitro and in vivo and its effect on apoptosis.Methods Cytotoxic effect of Pae on Eca-109 cells cultured in vitro was measured by MTT assay.Anti-tumor activity was performed on BALB/c nude mice xenografts model.The morphologic changes of tumor tissue were observed under light microscope and transmission electron microscope.The apoptosis index was assessed by TUNEL.Results Pae had significant in- hibitory effect on the proliferation of Eca-109 cells,and the IC50 value was 0.342 mmol?L-1.In the model of human esophageal cancer xenografts in BALB/c nude mice,the inhibitory rates of Pae group (25、50、100、200 mg?kg-1) were 10.67%、23.54%、27.91% and 34.46% respectively.In vivo administration of Pae 100 mg?kg-1 combined with cisplatin 5 mg?kg-1 resulted in a significant inhibition of Eca-109 tumor growth with the inhibitory rate of 77.91%,compared with cisplatin used alone (58.71%).The more apoptotic tumor cells could be seen under light microscope in every theraperutic groups than those in control.Changes of ultrastructure of tumor cells including concentration and side accumulation of the nuclear chromatin,and the fragmentation of the nuclear was observed under transmission electronic microscope.Apoptosis body was also found.The apoptosis indexes of every theraperutic groups were significantly different from the control.Conclusion Pae can inhibit the cell growth and induce apoptosis in human esophageal cancer cell line Eca-109 in vitro and in vivo.