scholarly journals Hesperetin inhibits Eca-109 cell proliferation and invasion by suppressing the PI3K/AKT signaling pathway and synergistically enhances the anti-tumor effect of 5-fluorouracil on esophageal cancer in vitro and in vivo

RSC Advances ◽  
2018 ◽  
Vol 8 (43) ◽  
pp. 24434-24443 ◽  
Author(s):  
Dandan Wu ◽  
Jiao Li ◽  
Xue Hu ◽  
Jingjing Ma ◽  
Weiguo Dong
Keyword(s):  
Cell Proliferation ◽  
Esophageal Cancer ◽  
Cancer Cells ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Anti Cancer ◽  
Esophageal Cancer Cells ◽  
Proliferation And Invasion

Effects of hesperetin on the proliferation and invasion of esophageal cancer cells and its synergistic anti-cancer effect with 5-FU.

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.

scholarly journals DPP3 Expression Promotes Cell Proliferation and Migration in Vitro and Tumor Growth in Vivo That Associates with Poor Prognosis of Esophageal Carcinoma

2021 ◽  
Author(s):  
Jing-Kun Liu ◽  
Abulizi Abudula ◽  
Hai-Tao Yang ◽  
Li-Xiu Xu ◽  
Ge Bai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Esophageal Cancer ◽  
Tumor Growth ◽  
Esophageal Carcinoma ◽  
Cancer Cells ◽  
Xenograft Model ◽  
Esophageal Cancer Cells ◽  
Tumor Growth And Invasion

Abstract Background: Dipeptidyl peptidase III (DPP3) is a zinc-dependent metallopeptidase and elevated in a variety of malignant tumors, but the underlying mechanism is not well understood so far. Here we investigated the association of esophageal carcinogenesis with the regulation of DPP3 expression by tissue-based quantitative analysis and the depletion of DPP3 expression in esophageal cancer cells and xenograft model. Methods: The expression level of DPP3 in esophageal cancer tissues and adjacent normal tissues was detected in 93 cases of tissue biopsies collected from patients diagnosed with esophageal carcinoma by immunohistochemistry. The effect of DPP3 expression on cell proliferation, migration or apoptosis was determined in DPP3-depleted esophageal cancer cells created by infection with the lentivirus containing the shRNA specific to human DPP3 mRNA sequence followed by cytometric detection using celigo cell count assay, flow cytometry, wound-healing assay and trans-well assay as well as chip screening with a Human Apoptosis Antibody Array kit, which enables the quantitative detection of 43 apoptosis-related genes. A xenograft model was applied to the detection of tumor growth and invasion of DPP3-depleted cancer cells in nude mice.Results: DPP3 expression was elevated in esophageal cancer tissues compared with adjacent non-tumor tissues (normal controls) with statistical significance (P<0.05), and associated with poor prognosis of esophageal carcinoma. The DPP3-depletion resulted in a reduced cell proliferation and migration and enhanced cell-cycle arrest and apoptosis of esophageal cancer cells, and lead to the inhibition of tumor growth and invasion in xenograft model. In addition, DPP3-depletion was associated with the upregulation of pro-apoptotic proteins and the downregulation of anti-apoptotic proteins.Conclusions: These findings suggest that DPP3 may promote cell proliferation, migration and survival of esophageal cancer cells in vitro, and tumor growth and invasion of esophageal carcinoma in vivo and this might serve as a molecular target for tumor therapy.

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 Cordycepin enhances the chemosensitivity of esophageal cancer cells to cisplatin by inducing the activation of AMPK and suppressing the AKT signaling pathway

2020 ◽  
Vol 11 (10) ◽  
Author(s):  
Ying Gao ◽  
Dan-Lei Chen ◽  
Mi Zhou ◽  
Zhou-san Zheng ◽  
Mei-Fang He ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Combination Therapy ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Caspase 3 ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Expression Levels ◽  
In Vivo Animal Model ◽  
Esophageal Cancer Cells

Abstract Although cisplatin (cDDP), is a first-line chemotherapy drug for esophageal cancer, it still has the potential to develop drug resistance and side effects. There is increasing evidence that cordycepin can work synergistically with other chemotherapy drugs. Therefore, we investigated whether combination therapy of cordycepin and cDDP may enhance the therapeutic effect of cDDP. We performed a series of functional tests to study the effect of medical treatment on esophageal cancer cells. We then used GO analysis to examine the pathways affected by treatment with cordycepin and cDDP. Next, we observed changes in the abundance of the selected pathway proteins. The in vivo animal model supported the results of the in vitro experiments. Co-treatment with cordycepin and cDDP inhibited cell growth, migration, and metastasis, as well as induced apoptosis. Cordycepin was found to effectively enhance activation of AMPK and inhibited activity of AKT. In all treatment groups, the expression levels of p-PI3K, p-Akt, p-p70S6K, Caspase-3, and Bcl-2 were significantly reduced, while the expression levels of p-AMPK, cleaved Caspase-3, and Bax increased, and the total levels of Akt, PI3K, and p70S6K levels remained unchanged. Overall, cordycepin was found to enhance the chemical sensitivity of esophageal cancer cells to cisplatin by inducing AMPK activation and inhibiting the AKT signaling pathway. Combination therapy of cordycepin and cisplatin represent a novel potential treatment of esophageal cancer.

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.

Lentivirus-Mediated RNA Interference Targeting the Long Noncoding RNA HOTAIR Inhibits Proliferation and Invasion of Endometrial Carcinoma Cells In Vitro and In Vivo

2014 ◽  
Vol 24 (4) ◽  
pp. 635-642 ◽  
Author(s):  
Jiaming Huang ◽  
Peiqi Ke ◽  
Luyan Guo ◽  
Wei Wang ◽  
Hao Tan ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Endometrial Cancer ◽  
Endometrial Carcinoma ◽  
Cancer Cells ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Proliferation And Invasion

ObjectiveThe overexpression of long noncoding RNA HOTAIR is associated with various aggressive solid carcinomas. However, its relationship with endometrial carcinoma has not been reported. The present study aimed to investigate the expression of the long noncoding RNA HOTAIR in endometrial carcinoma, its relationship with the carcinoma’s clinicopathologic features, and the biological function of HOTAIR in regulating endometrial cancer cell proliferation and invasion in vitro and in vivo.MethodsThe expression of HOTAIR was detected in different tissues and cell lines by real-time PCR. Lentivirus-mediated HOTAIR-specific shRNAvectors were transfected into endometrial cancer HEC-1A cells. Cell proliferation and colony formation were examined by CCK-8 assays and colony formation assays, respectively. Invasion and migration were examined by Transwell assays. Flow cytometry assay was used to examine the cell cycle. In addition, xenograft model assays were performed to analyze the growth of endometrial cancer cells in vivo.ResultsOur data showed that HOTAIR expression was higher in endometrial cancer cells and tissues than in normal endometrial tissues. HOTAIR expression was closely related to the tumor stage (P= 0.045), myometrial invasion (P= 0.014), and lymph node metastasis (P= 0.033). The down-regulation of HOTAIR resulted in a significant inhibition of cell proliferation, migration, and invasion and in cell cycle arrest at the G0/G1 phase. Furthermore, HOTAIR depletion significantly suppressed the endometrial cancer tumorigenesis in vivo.ConclusionsThis study is the first to suggest that HOTAIR plays an important role in the carcinogenesis of endometrial cancer. Targeting HOTAIR may be a novel therapeutic strategy for endometrial cancer.

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