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 Moscatilin Inhibits Growth of Human Esophageal Cancer Xenograft and Sensitizes Cancer Cells to Radiotherapy

2019 ◽  
Vol 8 (2) ◽  
pp. 187 ◽  
Author(s):  
Wun-Ke Chen ◽  
Chien-An Chen ◽  
Chih-Wen Chi ◽  
Li-Hui Li ◽  
Chin-Ping Lin ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Cell Counts ◽  
Blood Cell Counts ◽  
White Blood Cell Counts ◽  
Human Esophageal Cancer ◽  
Esophageal Cancer Cells ◽  
Plk1 Expression

Esophageal cancer prognosis remains poor in current clinical practice. We previously reported that moscatilin can induce apoptosis and mitotic catastrophe in esophageal cancer cells, accompanied by upregulation of polo-like kinase 1 (Plk1) expression. We aimed to validate in vitro activity and Plk1 expression in vivo following moscatilin treatment and to examine the treatment’s radiosensitizing effect. Human esophageal cancer cells were implanted in nude mice. Moscatilin was intraperitoneally (i.p.) injected into the mice. Tumor size, body weight, white blood cell counts, and liver and renal function were measured. Aberrant mitosis and Plk1 expression were assessed. Colony formation was used to measure survival fraction after radiation. Moscatilin significantly suppressed tumor growth in mice bearing human esophageal xenografts without affecting body weight, white blood cell counts, or liver and renal function. Moscatilin also induced aberrant mitosis and apoptosis. Plk1 expression was markedly upregulated in vivo. Moreover, moscatilin pretreatment enhanced CE81T/VGH and BE3 cell radioresponse in vitro. Moscatilin may inhibit growth of human esophageal tumors and sensitize esophageal cancer cells to radiation therapy.

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.

Effect of Suramin on Human Esophageal Cancer Cells in Vitro and in Vivo

1997 ◽  
Vol 32 (8) ◽  
pp. 824-828 ◽  
Author(s):  
R. Shin ◽  
Y. Naomoto ◽  
Y. Kamikawa ◽  
N. Tanaka ◽  
K. Orita
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Human Esophageal Cancer ◽  
Esophageal Cancer Cells

scholarly journals Radiosensitization of HER2-positive esophageal cancer cells by pyrotinib

2020 ◽  
Vol 40 (2) ◽  
Author(s):  
Xiangyao Lian ◽  
Cuimin Zhu ◽  
Haishan Lin ◽  
Zhengxing Gao ◽  
Guangxin Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Esophageal Cancer ◽  
Dna Repair ◽  
Cancer Cells ◽  
Cell Lines ◽  
Radiation Resistance ◽  
G1 Arrest ◽  
Her2 Positive ◽  
Proliferative Effect ◽  
Esophageal Cancer Cells

Abstract Radiation therapy is a widely used treatment for esophageal cancer. However, radiation resistance might result in a poor prognosis. Overexpression of HER2 has been related to adaptive radiation resistance. Pyrotinib is a HER2 inhibitor that shows an anti-tumor effect in breast cancer. The present study aims to explore the influence of pyrotinib combined with radiotherapy on HER2-positive esophageal cancer cells and explore the underlying mechanism. We screened two cell lines (TE-1 and KYSE30) that highly express HER2 from several human esophageal cancer cell lines. Cells were treated with pyrotinib or/and radiation. Cell proliferation, cell cycle distribution, and cell migration were measured. The protein levels involved in cell cycle and DNA repair were measured by Western blot. Results showed that pyrotinib inhibited HER2 activation and exerted an anti-proliferative effect in TE-1 and KYSE30 cells. Furthermore, it enhanced the anti-proliferative effect of radiation in these two cell lines. These effects might be via inhibiting HER2 phosphorylation, inducing G0/G1 arrest, and reducing EMT and DNA repair. Our results indicated that pyrotinib sensitivitied HER2 positive esophageal cancer cells to radiation treatment through various mechanisms. These findings may provide a new therapeutic strategy for treating HER2 positive esophageal cancer.

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.

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