Novel-miR-4885 Promotes Migration and Invasion of Esophageal Cancer Cells Through TargetingCTNNA2

2019 ◽  
Vol 38 (2) ◽  
pp. 151-161 ◽  
Author(s):  
Jing Song ◽  
Peng Zhang ◽  
Mengxin Liu ◽  
Ming Xie ◽  
Zhikui Gao ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Esophageal Cancer Cells

scholarly journals Aberrant hypermethylation-mediated downregulation of antisense lncRNA ZNF667-AS1 and its sense gene ZNF667 correlate with progression and prognosis of esophageal squamous cell carcinoma

2019 ◽  
Vol 10 (12) ◽  
Author(s):  
Zhiming Dong ◽  
Shengmian Li ◽  
Xuan Wu ◽  
Yunfeng Niu ◽  
Xiaoliang Liang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Cancer ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cancer Cells ◽  
Squamous Cell ◽  
Proximal Promoter ◽  
Migration And Invasion ◽  
Esophageal Cancer Cells ◽  
E Cadherin

AbstractNatural antisense lncRNAs can interfere with their corresponding sense transcript to elicit concordant or discordant regulation. LncRNA ZNF667-AS1 and its sense gene ZNF667 were found to be downregulated in esophageal squamous cell carcinoma (ESCC) tissues by RNA sequencing; however, the exact roles of both genes in ESCC occurrence and development have not been clarified. This study was to investigate the expression patterns, epigenetic inactivation mechanisms, function, and prognostic significance of ZNF667-AS1 and ZNF667 in ESCC tumorigenesis. Frequent downregulation of ZNF667-AS1 and ZNF667 was detected in esophageal cancer cells and ESCC tissues. The expression levels of ZNF667-AS1 and ZNF667 were significantly reversed by treatment with 5-Aza-dC and TSA in esophageal cancer cell lines. The CpG sites hypermethylation within proximal promoter influenced the binding ability of transcription factor E2F1 to the binding sites and then affected the transcription and expression of ZNF667-AS1 and ZNF667. Overexpression of ZNF667-AS1 and ZNF667 suppressed the viability, migration, and invasion of esophageal cancer cells in vitro. Overexpression of ZNF667-AS1 increased mRNA and protein expression level of ZNF667. ZNF667-AS1 interacts with and recruits TET1 to its target gene ZNF667 and E-cadherin to hydrolyze 5′-mc to 5′-hmc and further activates their expression, meanwhile, ZNF667-AS1 also interacts with UTX to decrease histone H3K27 tri-methylation to activate ZNF667 and E-cadherin expression. Furthermore, ZNF667-AS1 or ZNF667 expression and promoter methylation status were correlated with ESCC patients’ survival. Thus, these findings suggest that ZNF667-AS1 and ZNF667 may act as tumor suppressors and may serve as potential targets for antitumor therapy.

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 Knockdown of lncRNA TUC338 inhibits esophageal cancer cells migration and invasion

2021 ◽  
Vol 13 (5) ◽  
pp. 3061-3069
Author(s):  
Ting Qian ◽  
Hui Zhang ◽  
Shaorong Yu ◽  
Zhenzhang Chen ◽  
Hui Jia ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Esophageal Cancer Cells

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.

Increased miR-203-3p and reduced miR-21-5p synergistically inhibit proliferation, migration, and invasion in esophageal cancer cells

2019 ◽  
Vol 30 (1) ◽  
pp. 38-45 ◽  
Author(s):  
Yang Xia ◽  
Yihui Wang ◽  
Qi Wang ◽  
Maliha Ghaffar ◽  
Yuting Wang ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Esophageal Cancer Cells

Inhibition of Growth of Esophageal Cancer by Alantolactone via Wnt/βCatenin Signaling

2021 ◽  
Vol 21 ◽  
Author(s):  
Zijie Wang ◽  
Qing Hu ◽  
Huan Chen ◽  
Lei Shi ◽  
Min He ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Xenograft Model ◽  
Underlying Mechanism ◽  
Migration And Invasion ◽  
Colony Formation Assay ◽  
Crystal Violet Assay ◽  
Murine Xenograft Model ◽  
Anti Cancer ◽  
Esophageal Cancer Cells

Background: Alantolactone (AL) is a natural compound extracted from the roots of Inula Helenium L, which exerts an antitumor effect in a variety of cancer cell lines; however, its effect on esophageal cancer, a common malignancy with poor prognosis, remains unclear. Therefore, we aim to evaluate the effect of AL on esophageal cancer and to explore its underlying mechanism. Objective: This study aims to determine whether AL has an anti-cancer effect on esophageal cancer cells and to explore its underlying mechanism. Objective: This study aims to determine whether AL has an anti-cancer effect on esophageal cancer cells and to explore its underlying mechanism. Methods: The effect of AL on the proliferation and apoptosis of esophageal cancer cells was detected by MTT assay, colony formation assay, crystal violet assay, flow cytometry and hoechst apoptosis staining. The wound healing and Transwell invasion assay were performed to examine the effect of AL on the migration and invasion of esophageal cancer cells. Luciferase reporter system and Western blot were used to study the anti-tumor mechanism of AL on esophageal cancer cells. The subcutaneous murine xenograft model was employed to verify the effects of AL on esophageal cancer cells . Results: MTT assay, colony formation assay and crystal violet assay found that AL inhibited the growth of esophageal cancer cells. Hoechst staining and flow cytometry analysis showed that AL induced apoptosis in esophageal cancer through mitochondrial pathway. Transwell assay and wound healing assays showed that AL inhibited the metastasis and invasion of esophageal cancer cells. Wnt/ βcatenin signaling may contribute to the mechanism of the inhibition. The anti-tumor effect of AL on esophageal cancer cells was validated on murine xenograft model. Conclusion: Our data indicate that AL inhibits proliferation, migration, and invasion of esophageal cancer cells, and promotes apoptosis of esophageal cancer cells through the Wnt/β-catenin signaling pathway.

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