scholarly journals Pronounced Enhancement in Radiosensitization of Esophagus Cancer Cultivated in Docosahexaenoic Acid Via The PPAR-γ Activation

2021 ◽  
Author(s):  
Ying Yang ◽  
Ying Xu ◽  
Congzhao Zhao ◽  
Lirong Zhang ◽  
Aslibek Nuerbol ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Docosahexaenoic Acid ◽  
Cancer Cells ◽  
Combined Treatment ◽  
Strand Break ◽  
Ppar Γ ◽  
Squamous Cancer ◽  
Esophageal Cancer Cells

Abstract Background: Docosahexaenoic acid (DHA) has been reported to slow the tumor growth and improve prognosis, and been used to co-operate with many other chemotherapy medicines. Up to now, survey focuses on the interaction between DHA and radiation is relatively modest. Our study sought to evaluate the changes of radiosensitivity caused by DHA on esophageal cancer cells. Besides, potential mechanism and molecular are needed to be explored.Results：DHA enhanced proliferation inhibition of irradiation on esophageal cancer cells. DNA damage, especially double-strand break, induced by irradiation, was sharply increased by DHA addition. DHA accelerated G2/M phase blocking, cell apoptosis and lipid peroxidation after radiotherapy. The similar outcomings were observed in mouse xenograft tumor experiment that the malignancy substantially dismissed after the combined treatment of DHA and irradiation. Moreover, PPAR -γ was verified to increase post-treatment. Suppression of PPAR -γ would attenuate the radio sensitization triggered by DHA incompletely.Conclusion：DHA could improve radio sensitivity in esophageal squamous cancer cells in vivo and in vitro by activating PPAR -γ. Due to its explicitly usage and convenient, DHA and other PPAR -γ agonists would serve as an adjuvant therapy before radiotherapy if the clinical trials indicated positive from now on.

scholarly journals Dihydroartemisinin Increases the Sensitivity of Photodynamic Therapy Via NF-κB/HIF-1α/VEGF Pathway in Esophageal Cancer Cell in vitro and in vivo

2018 ◽  
Vol 48 (5) ◽  
pp. 2035-2045 ◽  
Author(s):  
Yanjing Li ◽  
Hong Sui ◽  
Cailing Jiang ◽  
Shumin Li ◽  
Yu Han ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Photodynamic Therapy ◽  
Cancer Cells ◽  
Cell Lines ◽  
Combined Treatment ◽  
Control Group ◽  
Vegf Pathway ◽  
Esophageal Cancer Cells

Background/Aims: Although photodynamic therapy (PDT) can relieve esophageal obstruction and prolong survival time of patients with esophageal cancer, it can induce nuclear factor-kappa B (NF-κB) activation in many cancers, which plays a negative role in PDT. Dihydroartemisinin (DHA), the most potent artemisinin derivative, can enhance the effect of PDT on esophageal cancer cells. However, the mechanism is still unclear. Methods: We generated stable cell lines expressing the super-repressor form of the NF-κB inhibitor IκBα and cell lines with lentivirus vector-mediated silencing of the HIF-1α gene. Esophageal xenograft tumors were created by subcutaneous injection of Eca109 cells into BALB/c nude mice. Four treatment groups were analyzed: a control group, photosensitizer alone group, light alone group, and PDT group. NF-κB expression was detected by an electrophoretic mobility shift assay, hypoxia-inducible factor α (HIF-1α) and vascular endothelial growth factor (VEGF) by real-time PCR, NF-κB, HIF-1α, and VEGF protein by western blot, and Ki-67, HIF-1α, VEGF, and NF-κB protein by immunohistochemistry. Results: PDT increased NF-κB activity and the gene expression of HIF-1α and VEGF in vitro and in vivo. In contrast, the DHA groups, particularly the combined DHA and PDT treatment group, abolished the effect. The combined treatment significantly inhibited tumor growth in vitro and in vivo. NF-κB activity and HIF-1α expression were also reduced in the stable IκBα expression group, whereas the former showed no change in HIF-1α-silenced cells. Conclusion: DHA might increase the sensitivity of esophageal cancer cells to PDT by inhibiting the NF-κB/HIF-1α/VEGF pathway.

scholarly journals Efficacy of Shikonin against Esophageal Cancer Cells and its possible mechanisms in vitro and in vivo

2018 ◽  
Vol 9 (1) ◽  
pp. 32-40 ◽  
Author(s):  
Jian-Cai Tang ◽  
Jia Zhao ◽  
Feng Long ◽  
Jian-ye Chen ◽  
Bo Mu ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Esophageal Cancer Cells

scholarly journals Sulforaphene induces apoptosis and inhibits the invasion of esophageal cancer cells through MSK2/CREB/Bcl-2 and cadherin pathway in vivo and in vitro

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Chengjuan Zhang ◽  
Junxia Zhang ◽  
Qiong Wu ◽  
Benling Xu ◽  
Guoguo Jin ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Biological Effects ◽  
Migration And Invasion ◽  
Global Changes ◽  
Fcm Analysis ◽  
Esophageal Cancer Cells

Abstract Background As a novel type of isothiocyanate derived from radish seeds from cruciferous vegetables, sulforaphene (SFE, 4-methylsufinyl-3-butenyl isothiocyanate) has various important biological effects, such as anti-oxidative and anti-bacterial effects. Recently, sulforaphene has attracted increasing attention for its anti-tumor effects and its ability to suppress the development of multiple tumors through different regulatory mechanisms. However, it has not yet been widely investigated for the treatment of esophageal cancer. Methods We observed an increased apoptosis in esophageal cancer cells on sulforaphene treatment through flow cytometry (FCM) analysis and transmission electron microscopy (TEM). Through mass spectrometry (MS) analysis, we further detected global changes in the proteomes and phosphoproteomes of esophageal cancer cells on sulforaphene treatment. The molecular mechanism of sulforaphene was verified by western blot,the effect and mechanism of SFE on esophageal cancer was further verified by patient-derived xenograft mouse model. Results We identified multiple cellular processes that were changed after sulforaphene treatment by proteomics. We found that sulforaphene could repress the phosphorylation of CREB through MSK2, leading to suppression of Bcl-2 and further promoted cell apoptosis. Additionally, we confirmed that sulforaphene induces tumor cell apoptosis in mice. Interestingly, we also observed the obvious inhibition of cell migration and invasion caused by sulforaphene treatment by inhibiting the expression of cadherin, indicating the complex effects of sulforaphene on the development of esophageal cancer. Conclusions Our data demonstrated that sulforaphene induced cell apoptosis and inhibits the invasion of esophageal cancer through a mechanism involving the inhibition of the MSK2–CREB–Bcl2 and cadherin pathway. Sulforaphene could therefore serve as a promising anti-tumor drug for the treatment of esophageal cancer.

scholarly journals Effects and Mechanisms of Metformin on the Proliferation of Esophageal Cancer Cells In Vitro and In Vivo

2017 ◽  
Vol 49 (3) ◽  
pp. 778-789 ◽  
Author(s):  
Jian-Cai Tang ◽  
Rui An ◽  
Yi-Qing Jiang ◽  
Jian Yang
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Esophageal Cancer Cells

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.

scholarly journals Ribophorin II promotes cell proliferation, migration, and invasion in esophageal cancer cells in vitro and in vivo

2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Yongshun Li ◽  
Changrong Huang ◽  
Qizhou Bai ◽  
Jun Yu
Keyword(s):  
Cell Proliferation ◽  
Esophageal Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Cancer Tissues ◽  
Esophageal Cancer Cells ◽  
E Cadherin

AbstractEsophageal cancer is a common digestive tract cancer, which is a serious threat to human health. Ribophorin II (RPN2) is a part of an N-oligosaccharyltransferase complex, which is excessively expressed in many kinds of cancers. In the present study, we explore the biological role of RNP2 in esophageal cancer. First, we found that the expression of RPN2 was higher in esophageal cancer tissues than in adjacent non-tumor tissues, and negatively correlated with E-cadherin expression. RPN2 expression levels in esophageal cancer tissues were positively associated with differentiation and tumor node metastasis (TNM) stage. Furthermore, the expression of RPN2 was increased significantly in esophageal cancer cell lines compared with normal cells. The effect of RPN2 down-regulation on cell proliferation, cell migration, and cell invasion was examined by cell counting kit-8 (CCK8), wound healing assay, and Transwell assay, respectively. Silencing RPN2 effectively inhibited cell proliferation of esophageal cancer cells in vitro and in vivo. Cell migration and invasion were also weakened dramatically by siRPN2 treatment of esophageal cancer cells. In addition, protein expression of proliferating cell nuclear antigen (PCNA), matrix metalloproteinase (MMP-2), and E-cadherin in esophageal cancer cells was determined by Western blot analysis. PCNA, MMP-2, E-cadherin, Snail and phosphorylation-Smad2/3 expression was also regulated notably by siRPN2 treatment. These findings indicate that RPN2 exhibits oncogenetic capabilities in esophageal cancer, which could provide novel insights into esophageal cancer prevention and 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 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.

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