scholarly journals Mannose enhances the radio-sensitivity of esophageal squamous cell carcinoma with low MPI expression by suppressing glycolysis

2022 ◽  
Vol 13 (1) ◽  
Author(s):  
Hui Luo ◽  
Xiaohui Wang ◽  
Yunhan Wang ◽  
Qinfu Dan ◽  
Hong Ge
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Cell Line ◽  
Cell Lines ◽  
Inhibitory Effect ◽  
Esophageal Cancer Cell ◽  
Human Esophageal Cancer ◽  
Radio Sensitivity ◽  
Esophageal Cancer Cells ◽  
Kyse450 Cell

Abstract Background To investigate the effect of mannose on radio-sensitivity of human esophageal squamous cell carcinoma (ESCC) cell line and its possible mechanism. Methods The expression of mannose phosphate isomerase (MPI) in human esophageal cancer cell lines were detected by Western blot. The inhibitory effect of mannose on human esophageal cancer cell lines were observed by MTT assay. Plate clone formation assay was performed to investigate the efficacy of mannose on radio-sensitivity of human esophageal cancer cells. The apoptosis rates of tumor cells treated with mannose and/or radiation therapy was calculated by flow cytometry. Furthermore, we analyzed intracellular metabolites using liquid chromatography mass spectrometry to identify selective sugar metabolites. Results MPI expression was various in human esophageal cancer cells. KYSE70 cells was associated with the highest MPI expression whereas KYSE450 cells had the lowest MPI expression level. When administrated with 11.1 mM/L mannose, the same inhibitory effect was observed in both KYSE70 and KYSE450 cell lines. Moreover, the inhibitory effect was significant on KYSE450 cell lines with an increased mannose concentration. The application of 11.1 mM/L mannose could significantly enhance the radio-sensitivity of KYSE450 cell line; and tumor cell apoptosis rate was also increased. However, there was limited efficacy of mannose on the radio-sensitivity and apoptosis rate of KYSE70 cell line. Additionally, intracellular metabolites analyzation revealed that glycolysis could be disturbed by mannose when combined with radiation therapy in esophageal cancer cells. Conclusion In esophageal cancer cell lines with low MPI expression, the administration of mannose was associated with enhanced radio-sensitivity.

scholarly journals Anticancer Effects of Dihydroartemisinin on Human Esophageal Cancer Cells In Vivo

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Cailing Jiang ◽  
Shumin Li ◽  
Yanjing Li ◽  
Yuxian Bai
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Dependent Manner ◽  
Esophageal Cancer Cell ◽  
Human Esophageal Cancer ◽  
Semisynthetic Derivative ◽  
Esophageal Cancer Cells ◽  
Dose Dependent

Despite recent advances in chemotherapy and surgical resection, the 5-year survival rate of esophageal cancer still remains at the low level. Therefore, it is very important to discover a new agent to improve the life expectancy of patients with esophageal cancer. Dihydroartemisinin (DHA), a semisynthetic derivative of artemisinin, has recently exhibited promising anticancer activity against various cancer cells. But so far, the specific mechanism remains unclear. We have previously demonstrated that DHA reduced viability of esophageal cancer cells in a dose-dependent manner in vitro and induced cell cycle arrest and apoptosis. Here, we extended our study to further observe the efficacy of DHA on esophageal cancer cells in vivo. In the present study, for the first time, we found that DHA significantly inhibits cell proliferation in xenografted tumor compared with the control. The mechanism was that DHA induced cell apoptosis in both human esophageal cancer cell lines Eca109 and Ec9706 in vivo in a dose-dependent manner. The results suggested that DHA was a promising agent against esophageal cancer in the clinical treatment.

Oncolytic adenovirus expressing apoptotic genes targets radiation resistant (RR) esophageal cancer

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 21043-21043
Author(s):  
J. Y. Chang ◽  
R. Komaki ◽  
X. Zhang ◽  
L. Wang ◽  
B. Fang
Keyword(s):  
Gene Expression ◽  
Esophageal Cancer ◽  
Radiation Exposure ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Esophageal Cancer Cell ◽  
Esophageal Cancer Cells ◽  
Trans Gene ◽  
Fractionated Radiation

21043 Background: Only 25% of esophageal cancer patients achieve pathological complete response after standard chemoradiotherapy. Radiation dose escalation is associated with higher toxicity but no therapeutic improvement. In addition, esophageal cancer cells may develop radiation resistance (RR) after fractionated radiation exposure. Therefore, molecular targeting therapy for RR esophageal cancer is urgently needed. Methods: Six pairs of RR esophageal cancer cell lines were established by applying continuous 2 Gy fractionated irradiation. Ad/TRAIL-E1, an oncolytic adenoviral vector expressing both apoptotic TRAIL and viral E1A genes under the control of tumor specific human telomerase reverse transcriptase promoter, was constructed. Phosphate buffer solution and vectors expressing the TRAIL gene only, the GFP marker protein only, or the E1A gene only served as controls. Trans-gene expression, apoptosis activation, and the RR esophageal cancer cells targeted were evaluated in vitro and in vivo. A human esophageal RR cancer model was established and locally treated with Ad/TRAIL-E1 or controls. Results: After fractionated radiation exposure, esophageal cancer cell lines developed RR (up to 25-fold) that was associated with activation of the anti-apoptotic pathway. Ad/TRAIL-E1 activated an apoptotic cascade of caspases and selectively killed esophageal cancer cells but not normal cells. Ad/TRAIL-E1 preferentially targeted RR stem-like cancer cells with higher trans-gene expression and cell killing compared with parental cells. Overexpression (3 times) of Coxsackie's and adenoviral receptors in RR esophageal cancer cells compared with parental cells was noted. Ad/TRAIL-E1 therapy resulted in 40% tumor-free survival without the treatment- related toxicity found in human RR esophageal adenocarcinoma mouse models (p<0.05 as compared with controls). Conclusions: Esophageal cancer cells develop RR after fractionated radiation exposure. Ad/TRAIL-E1 preferentially targeted RR stem-like esophageal cancer cells, which resulted in a 40% cure rate. No significant financial relationships to disclose.

scholarly journals Therapeutic and Radiosensitizing Effects of Armillaridin on Human Esophageal Cancer Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Chih-Wen Chi ◽  
Chien-Chih Chen ◽  
Yu-Jen Chen
Keyword(s):  
Cell Cycle ◽  
Esophageal Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Transmembrane Potential ◽  
Mitochondrial Transmembrane Potential ◽  
Cell Counts ◽  
Human Esophageal Cancer ◽  
Esophageal Cancer Cells

Background. Armillaridin (AM) is isolated fromArmillaria mellea. We examined the anticancer activity and radiosensitizing effect on human esophageal cancer cells.Methods. Human squamous cell carcinoma (CE81T/VGH and TE-2) and adenocarcinoma (BE-3 and SKGT-4) cell lines were cultured. The MTT assay was used for cell viability. The cell cycle was analyzed using propidium iodide staining. Mitochondrial transmembrane potential was measured by DiOC6(3) staining. The colony formation assay was performed for estimation of the radiation surviving fraction. Human CE81T/VGH xenografts were established for evaluation of therapeutic activityin vivo.Results. AM inhibited the viability of four human esophageal cancer cell lines with an estimated concentration of 50% inhibition (IC50) which was 3.4–6.9 μM. AM induced a hypoploid cell population and morphological alterations typical of apoptosis in cells. This apoptosis induction was accompanied by a reduction of mitochondrial transmembrane potential. AM accumulated cell cycle at G2/M phase and enhanced the radiosensitivity in CE81T/VGH cells.In vivo, AM inhibited the growth of CE81T/VGH xenografts without significant impact on body weight and white blood cell counts.Conclusion. Armillaridin could inhibit growth and enhance radiosensitivity of human esophageal cancer cells. There might be potential to integrate AM with radiotherapy for esophageal cancer treatment.

scholarly journals Characteristics of P-Type and N-Type Photoelectrochemical Biosensors: A Case Study for Esophageal Cancer Detection

Nanomaterials ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 1065
Author(s):  
Joseph-Hang Leung ◽  
Hong-Thai Nguyen ◽  
Shih-Wei Feng ◽  
Sofya B. Artemkina ◽  
Vladimir E. Fedorov ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Carrier Transport ◽  
X Ray Diffraction ◽  
Photoelectrochemical Response ◽  
Carrier Separation ◽  
Human Esophageal Cancer ◽  
P Type ◽  
Esophageal Cancer Cells

P-type and N-type photoelectrochemical (PEC) biosensors were established in the laboratory to discuss the correlation between characteristic substances and photoactive material properties through the photogenerated charge carrier transport mechanism. Four types of human esophageal cancer cells (ECCs) were analyzed without requiring additional bias voltage. Photoelectrical characteristics were examined by scanning electron microscopy (SEM), X-ray diffraction (XRD), UV–vis reflectance spectroscopy, and photocurrent response analyses. Results showed that smaller photocurrent was measured in cases with advanced cancer stages. Glutathione (L-glutathione reduced, GSH) and Glutathione disulfide (GSSG) in cancer cells carry out redox reactions during carrier separation, which changes the photocurrent. The sensor can identify ECC stages with a certain level of photoelectrochemical response. The detection error can be optimized by adjusting the number of cells, and the detection time of about 5 min allowed repeated measurement.

Epigenetic modulation combined with PD-1/PD-L1 blockade enhances immunotherapy based on MAGE-A11 antigen-specific CD8+T cells against esophageal carcinoma

2020 ◽  
Vol 41 (7) ◽  
pp. 894-903
Author(s):  
Yunyan Wu ◽  
Meixiang Sang ◽  
Fei Liu ◽  
Jiandong Zhang ◽  
Weijing Li ◽  
...  
Keyword(s):  
T Cells ◽  
Esophageal Cancer ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cd8 T Cells ◽  
Dna Methyltransferase ◽  
Tumor Cell Lines ◽  
Epigenetic Modulation ◽  
Esophageal Cancer Cells

Abstract Cancer testis antigens (CTAs) are promising targets for T cell-based immunotherapy and studies have shown that certain CT genes are epigenetically depressed in cancer cells through DNA demethylation. Melanoma-associated antigen A11 (MAGE-A11) is a CTA that is frequently expressed in esophageal cancer and is correlated with a poor esophageal cancer prognosis. Consequently, MAGE-A11 is a potential immunotherapy target. In this study, we evaluated MAGE-A11 expression in esophageal cancer cells and found that it was downregulated in several tumor cell lines, which restricted the effect of immunotherapy. Additionally, the specific recognition and lytic potential of cytotoxic T lymphocytes (CTLs) derived from the MAGE-A11 was determined. Specific CTLs could kill esophageal cancer cells expressing MAGE-A11 but rarely lysed MAGE-A11-negative tumor cells. Therefore, induction of MAGE-A11 expression is critical for CTLs recognition and lysis of esophageal cancer cells. Treatment with the DNA methyltransferase inhibitor 5-aza-2′-deoxycytidine increased MAGE-A11 expression in esophageal cancer cells and subsequently enhanced the cytotoxicity of MAGE-A11-specific CD8+T cells against cancer cell lines. Furthermore, we found that PD-L1 expression in esophageal cancer cells affected the antitumor function of CTLs. programmed death-1 (PD-1)/PD-L1 blockade could increase the specific CTL-induced lysis of HLA-A2+/MAGE-A11+ tumor cell lines treated with 5-aza-2′-deoxycytidine. These findings indicate that the treatment of tumor cells with the DNA methyltransferase inhibitor 5-aza-2′-deoxycytidine augments MAGE-A11 expression in esophageal cancer cells. The combination of epigenetic modulation by 5-aza-2′-deoxycytidine and PD-1/PD-L1 blockade may be useful for T cell-based immunotherapy against esophageal cancer.

Bioactivities of Sophorolipid with Different Structures Against Human Esophageal Cancer Cells

2012 ◽  
Vol 173 (2) ◽  
pp. 286-291 ◽  
Author(s):  
Lingjian Shao ◽  
Xin Song ◽  
Xiaojing Ma ◽  
Hui Li ◽  
Yinbo Qu
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Human Esophageal Cancer ◽  
Esophageal Cancer Cells
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