Human Esophageal Carcinoma Eca-109 Cells Research Articles

Retracted] Talen‑mediated girdin knockout downregulates cell proliferation, migration and invasion in human esophageal carcinoma ECA109 cells.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that the Transwell cell migration data shown in Fig.6 were strikingly similar to data appearing in different form in other articles by different authors; furthermore, there were other possible anomalies associated with these data. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 10: 848‑854, 2014; DOI: 10.3892/mmr.2014.2268].

Silence of cZNF292 suppresses the growth, migration, and invasion of human esophageal cancer Eca-109 cells via upregulating miR-206.

Circular RNA (circRNA) cZNF292 has been previously revealed as a circular oncogenic RNA. This study attempted to illustrate the functions of cZNF292 in human esophageal carcinoma Eca-109 cells. Eca-109 cells were transfected with the short hairpin RNA specific against cZNF292 (sh-cZNF292) and/or miR-206 inhibitor. cZNF292 and miR-206 expression was examined by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). Cell counting kit-8 and flow cytometry were performed for detecting cell growth including cell viability as well as apoptosis. Various kinds of factors, which are involved in cell development including proliferation, apoptosis, migration, and invasion were determined by western blot analysis. Besides, the activation of AMP-activated protein kinase (AMPK) and PI3K/AKT signaling was measured by western blot analysis. It was found that cZNF292 silencing decreased Eca-109 cell viability and induced apoptosis. In the meantime, cZNF292 silencing inhibited cell migration and invasion. cZNF292 silencing upregulated miR-206 expression. And miR-206 downregulation impaired the suppressive effects of cZNF292 silence toward Eca-109 cell growth, migration, and invasion. cZNF292 silencing activated AMPK signaling and inactivated PI3K/AKT signaling also via regulating miR-206. In conclusion, silencing of cZNF292 abated growth, migration, and invasion of Eca-109 cells by upregulating miR-206, which subsequently modulated AMPK and PI3K/AKT signaling pathways.

Mechanism of Oxymatrine-induced Human Esophageal Cancer Cell Apoptosis by the Endoplasmic Reticulum Stress Pathway.

Endoplasmic reticulum stress is one of the mechanisms of cell apoptosis. In this study, the mechanism of oxymatrine-induced human esophageal cancer Eca-109 cell apoptosis by the endoplasmic reticulum stress pathway was investigated. Eca-109 cells were cultured in vitro with different doses of oxymatrine (0.5, 1, 2 μg/mL) for 48 h. The cell viability and proliferation inhibition rate were examined by MTT assay and cell cycle assay. The apoptosis rate was examined by Annexin V-FITC/propidium iodide assay. The expression of endoplasmic reticulum stress markers, including binding immunoglobulin protein and CCAAT-enhancer-binding protein homologous protein, were determined by real-time quantitative polymerase chain reaction and western blotting, respectively. MTT data showed that oxymatrine significantly inhibited the proliferation of Eca-109 cells. The cell apoptosis rate was quantified by flow cytometry. The expression of binding immunoglobulin protein was markedly downregulated in oxymatrine-treated Eca-109 cells while that of CCAAT-enhancer-binding protein homologous protein was upregulated. Oxymatrine inhibited proliferation and induced apoptosis of human esophageal carcinoma Eca-109 cells. Thus, oxymatrine may be a potential agent for treating human esophageal cancer.

Bufalin induces apoptosis in human esophageal carcinoma ECA109 cells by inhibiting the activation of the mTOR/p70S6K pathway.

The present study examined whether bufalin could induce human esophageal carcinoma ECA109 cells apoptosis via inhibiting the activation of mechanistic target of rapamycin (mTOR)/p70 S6 kinase (p70S6K) pathway is discussed in this article. The present study used the esophageal squamous cell carcinoma ECA109 cell line to assess the apoptosis-inducing effects of bufalin via inhibition of the mTOR/p70S6K pathways. A plasmid containing the wild-type mTOR gene (wtmTOR) was transfected into ECA109 cells. The levels of p70S6K, phosphorylated (p)-p70S6K, cellular inhibitor of apoptosis-1 (cIAP-1) and Bcl-2-associated death promoter (BAD) in ECA109 cells were examined by western blot analysis, and apoptosis was detected by flow cytometry analysis and Giemsa staining. The results revealed that the expression of p-p70S6K was increased as the time progressed (at 0, 12 and 24 h), and then decreased at 30, 36, 42 and 48 h after transfection. The expression of cIAP-1 was significantly decreased as time progressed following the addition of bufalin, whereas that of BAD was increased. The levels of p-p70S6K and cIAP-1 were significantly higher in the wtmTOR-transfected group than in the control and empty vector-transfected groups, and then reduced following addition of bufalin; however, BAD expression was significantly lower in the wtmTOR-transfected group. The results of flow cytometry revealed the cell cycle of ECA109 was arrested at G2/M phase and the apoptotic rate was significantly lower in the wtmTOR-transfected group than in the control and empty vector-transfected groups, and then increased following addition of bufalin. In conclusion, the findings of the present study demonstrated that bufalin induced apoptosis in esophageal carcinoma cells via the inhibition of the mTOR/p70S6K pathway and indicated that treatment with bufalin could be combined with chemotherapy to overcome the resistance of esophageal carcinoma cells to chemotherapeutic-induced apoptosis.

Effect of lentivirus-mediated expression of RNF2 gene on the proliferation and migration of esophageal carcinoma cells following X-ray radiotherapy

Objective To examine the effect of X-ray radiotherapy on cell proliferation, migration, apoptosis, and cell cycle of human esophageal carcinoma ECA-109 cells following RNA interference (RNAi)-mediated downregulation of RNF2 gene expression. Methods The level of RNF2 mRNA expression in the human esophageal carcinoma cell line ECA-109 was determined using RT-PCR. Cell proliferation of ECA-109 was measured by MTT assay, and the changes in RNF2 protein expression in ECA-109-R cells were determined using Western blot. The changes in cell cycle and cell apoptosis at different time points following radiation were analyzed by flow cytometry, and the effect of transduction on cell migration was examined using Transwell migration assay. Data were subjected to an analysis of variance with repeated measurement design. Results The mean mRNA and protein levels of RNF2 in ECA-109 cells were significantly increased in a dose-dependent manner in the radiation group than in the control group (P 0.05). The Transwell migration assay showed that the number of migrating cells following 3.5 h of radiation was significantly lower in the ECA-109-R group than in the ECA-109 and ECA-109-N groups (P<0.01). The percentage of G2/M phase cells in each group was significantly lower following 6 Gy radiation compared to that in the corresponding untreated group (P<0.01), and the percentage of G2/M phase cells was significantly lower in the ECA-109-R group than in the ECA-109 and ECA-109-N groups (P<0.05). Furthermore, cell apoptosis following radiation was also significantly higher in the ECA-109-R group than in the ECA-109 and ECA-109-N groups (P<0.01). Conclusions RNAi-mediated downregulation of RNF2 expression in esophageal carcinoma cells can reduce cell proliferation and cell migration, rescue post-radiation G2/M cell cycle arrest, promote cell apoptosis, and increase radiosensitivity. Key words: RNF2 gene; Cell proliferation; Apoptosis; Cell cycle; Esophageal carcinoma cell line

DADS suppresses human esophageal xenograft tumors through RAF/MEK/ERK and mitochondria-dependent pathways.

Diallyl disulfide (DADS) is a natural organosulfur compound isolated from garlic. DADS has various biological properties, including anticancer, antiangiogenic, and antioxidant effects. However, the anticancer mechanisms of DADS in human esophageal carcinoma have not been elucidated, especially in vivo. In this study, MTT assay showed that DADS significantly reduced cell viability in human esophageal carcinoma ECA109 cells, but was relatively less toxic in normal liver cells. The pro–apoptotic effect of DADS on ECA109 cells was detected by Annexin V-FITC/propidium iodide (PI) staining. Flow cytometry analysis showed that DADS promoted apoptosis in a dose-dependent manner and the apoptosis rate could be decreased by caspase-3 inhibitor Ac-DEVD-CHO. Xenograft study in nude mice showed that DADS treatment inhibited the growth of ECA109 tumor in both 20 and 40 mg/kg DADS groups without obvious side effects. DADS inhibited ECA109 tumor proliferation by down-regulating proliferation cell nuclear antigen (PCNA). DADS induced apoptosis by activating a mitochondria-dependent pathway with the executor of caspase-3, increasing p53 level and Bax/Bcl-2 ratio, and downregulating the RAF/MEK/ERK pathway in ECA109 xenograft tumosr. Based on studies in cell culture and animal models, the findings here indicate that DADS is an effective and safe anti-cancer agent for esophageal carcinoma.

Talen-mediated girdin knockout downregulates cell proliferation, migration and invasion in human esophageal carcinoma ECA109 cells

Girdin is an actin-binding Akt substrate that is involved in the regulation of cell migration. Accumulating evidence has revealed that girdin has regulatory effects on invasion and metastasis in several types of cancer. However, the role of girdin in esophageal squamous cell carcinomas (ESCCs) is yet to be investigated. In the present study, tissue microarray data revealed that among 95cases of ESCC, 27cases (28.7%) exhibited a low expression of girdin, while 67cases (71.3%) had an enhanced expression of girdin. However, among 78cases of adjacent tissues, 64cases (82.1%) did not express girdin and 14cases (17.9%) exhibited a low expression of girdin. Furthermore, the expression of girdin was significantly associated with the tumor stage, lymph node metastasis stage, and tumor, lymph node and metastasis stage. Of note, the mean survival time of girdin-positive cases was only 30.62±2.99months, while it was 53.37±5.02 months in girdin-negative cases, indicating that girdin protein expression is an independent prognostic factor of poor survival. Talen-mediated girdin knockout (KO) significantly suppressed cellular proliferation, migration and invasion in ESCC ECA109cells. In conclusion, the present study suggested that girdin protein expression was significantly correlated with cancer progression and poor prognosis in ESCCs, and that girdin had a positive role in the regulation of cell proliferation, migration and invasion in ESCC cells. Therefore, girdin may be a potential candidate for the development of novel prognostic tools and therapeutic strategies for ESCCs.

Effect of TSLC1 gene on growth and apoptosis in human esophageal carcinoma Eca109 cells

IntroductionTo explore the effect of tumor suppressor in lung cancer 1 (TSLC1) on proliferation and apoptosis in esophageal cancer Eca109 cells.Material and methodsEca109 cells were divided into three groups: TSLC1 transfected group (TTG), mock group (MG) and untransfected group (UTG). The TTG and MG were transfected transiently with the pIRES2-EGFP-TSLC1 eukaryotic expression vector and pIRES2-EGFP vector respectively. The UTG was a blank control. The TSLC1 expression in TTG was analyzed with the fluorogram and RT-PCR method. Cell proliferation was measured with 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium (MTT) assay. Cell cycle was measured by flow cytometry (FCM). Cell apoptosis was detected by Annexin-V/PI double staining FCM.ResultsGreen color was found in TTG and MG. The band of TSLC1 mRNA of TTG was located at about 1400 bp by RT-PCR and agarose gel electrophoresis assay. The TSLC1 inhibited cell proliferation significantly in MTT assay, and the cell proliferation was slower in TTG than MG and UTG. After TSLC1 transfection, cell numbers increased in G0/G1 phase and decreased in S phase. Forty-eight hours after transfection, the apoptosis rate and death rate of TTG were higher than MG and UTG. Thus TSLC1 induced Eca109 cells to apoptosis.ConclusionsThe TSLC1 gene had a potent effect on cell proliferation inhibition, G1/S cell cycle arrest and induction of cell apoptosis in Eca109 cells.

Effects of Oxymatrine on the apoptosis of human esophageal carcinoma Eca109 cell line and its mechanism

The effects of Oxymatrine (Oxy) on the proliferation and apoptosis of human esophageal carcinoma Eca109 cell line and the mechanism were investigated. The human esophageal carcinoma Eca109 cells were cultured in vitro. The Oxy-induced apoptosis of Eca 109 cells was assayed by using flow cytometry. The expressions of p-ERK(1/2), Cyclin D1, p21(waf/cip1), Bax and Bcl-2 were detected by Western blot. Flow cytometry revealed that Oxy could induce the apoptosis of Eca109 cells. Western blot showed that Oxy of different concentrations suppressed the expressions of p-ERK(1/2), Cyclin D1 and Bcl-2, but up-regulated the expression of p21(waf/cip1) and Bax, and the ratio of Bax/Bcl-2 was increased. It was suggested the Oxy could induce the apoptosis of Eca109 cells, which might be related to the upregulation of p21(waf/cip1) and the downregulation of p-ERK(1/2), Cyclin D1 and p21(waf/cip1). The possible pathway may be related to Bcl-2/Bax.

Expression of IL 1betaconverting enzyme in 5-FU induced apoptosis in esophageal carcinoma cells.

AIM:To study the role of interleukin 1beta converting enzyme(ICE)in antitumor drug induced apoptosis in tumor cells.METHODS:Morphological changes in human esophageal carcinoma Eca-109 cells after treated with 5-fluorouracil (5-FU) were observed under light and electron microscope. Expression of ICE in the tumor cells exposed to 5-FU was examined by the immunocytochemical method.RESULTS:The cells treated with 5-FU displayed disappearance of nucleoli, chromatin gathering under nuclear envelope, karyorrhexis, budding and the formation of apoptotic bodies.The expression of ICE was negative in control cells, and 5-FU could induce the ICE expression in Eca-109 cells undergoing apoptosis. The number and the staining intensity of positive cells increased with the extension of action time.CONCLUSION: 5-FU may induce apoptosis in human esophageal carcinoma Eca-109 cells; ICE gene may be involved in the regulation of 5-FU induced apoptosis; and ICE protein may mediate apoptosis induced by 5-FU.