scholarly journals X-linked inhibitor of apoptosis protein accelerates migration by inducing epithelial–mesenchymal transition through TGF-β signaling pathway in esophageal cancer cells

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Yuxiang Jin ◽  
Xinye Lu ◽  
Mingdong Wang ◽  
Xuewei Zhao ◽  
Lei Xue
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Inhibitor Of Apoptosis ◽  
Mesenchymal Transition ◽  
Inhibitor Of Apoptosis Protein ◽  
Apoptosis Protein ◽  
Esophageal Cancer Cells ◽  
Emt Markers

Abstract Background The prognosis of esophageal cancer is still dismal because of its high probability of metastasis that is likely related to the cellular process of epithelial–mesenchymal transition (EMT). Recent studies have shown a novel role of X-linked inhibitor of apoptosis protein (XIAP) in regulating the migration process of cancer cells and, therefore, linking to progression and poor prognosis of cancer. Methods The expression of XIAP in esophageal squamous cell cancer (ESCC) tissues was determined by immunohistochemistry assay. Cell migration was analyzed by wound healing assay and Transwell assay. The expression of EMT markers (E-cadherin, N-cadherin and Vimentin) was revealed by immunofluorescence assay. Quantitative real‑time PCR analysis and Western blot analysis were used to detect the expression of XIAP and EMT markers as well as transforming growth factor-β (TGF-β) at mRNA and protein level, respectively. Results We found that the expression of XIAP closely correlated to the probability of lymphatic metastasis in patients and that ESCC patients with the high XIAP expression were associated with worse overall survival (OS). Univariate and multivariate analysis also revealed XIAP as an independent prognostic factor for overall survival in ESCC patients. In both EC9706 and TE13 cell lines, knockdown of XIAP decreased the migration of cancer cells by inhibiting EMT process through regulating the TGF-β signaling pathway, pinpointing a regulatory role of XIAP in migratory process upon TGF-β activation. Conclusions Taken together, our results suggest XIAP as a important prognostic and regulative factor in ESCC patients. XIAP may promote migration of esophageal cancer cells through the activation of TGF-β mediated EMT.

scholarly journals EMT Participates in the Regulation of Exosomes Secretion and Function in Esophageal Cancer Cells

2021 ◽  
Vol 20 ◽  
pp. 153303382110330
Author(s):  
Chuangui Chen ◽  
Zhao Ma ◽  
Hongjing Jiang
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Promoting Effect ◽  
Migration Ability ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration ◽  
And Function ◽  
Esophageal Cancer Cells

Epithelial-mesenchymal transition (EMT) is a key step in tumor invasion and distant metastasis. Abundant evidence has documented that exosomes can mediate EMT of tumor cells and endow them with the ability of invasion and migration. However, there are few studies focusing on whether EMT can reverse the secretion of exosomes. In this study, 2 esophageal cancer cells (FLO-1 and SK-GT-4) were selected to compare the migration ability and EMT activation, and to further analyze the secretion ability of exosomes of the 2 cell lines. According to the results, inhibited activation of EMT in FLO-1 cells with relatively high migration ability could effectively reduce the secretion of exosomes. Besides, in SK-GT-4 cells, EMT activation induced by TGF-β could promote the secretion of exosomes. FLO-1 cell derived exosomes exhibited a paracrine effect of promoting the migration of SK-GT-4 cells, and the use of EMT inhibitors could weaken this ability. Furthermore, inhibition of EMT could change the relative content of some miRNAs in exosomes, with a particularly significant downregulation in the expression of miR-196-5p, miR-21-5p and miR-194-5p. Significantly, artificial transfection of the 3 miRNAs into exosomes by electroporation resulted in the recovery of migration-promoting effect of exosomes. Subsequent experiments further revealed that the effect of EMT on these miRNAs could be explained by the intracellular transcription level or the specific sorting mechanism of exosomes. To sum up, our study undoubtedly reveals that EMT has a regulatory effect on exosomes in the quantity and contents in esophageal cancer cells. Significantly, findings in our study provide experimental evidence for the interaction of EMT with the secretion and sorting pathway of exosomes, and also give a new direction for the further study of tumor metastasis.

scholarly journals [ARTICLE WITHDRAWN] MicroRNA-539 Inhibits the Epithelial‐Mesenchymal Transition of Esophageal Cancer Cells by Twist-Related Protein 1-Mediated Modulation of Melanoma-Associated Antigen A4

2018 ◽  
Vol 26 (4) ◽  
pp. 529-536 ◽  
Author(s):  
Zhili Cao ◽  
Xiang Zheng ◽  
Lei Cao ◽  
Naixin Liang
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
The United States ◽  
Research Data ◽  
Original Study ◽  
Related Protein ◽  
Mesenchymal Transition ◽  
Scientific Nature ◽  
Esophageal Cancer Cells

This article has been withdrawn at the request of the author in December 2020. STATEMENT FOR WITHDRAWAL OF MANUSCRIPT FROM ONCOLOGY RESEARCH Dear Editors, I am Dr. Naixin Liang. For some scientific reasons, my team and I are very sorry to apply to withdraw the manuscript "MicroRNA-539 Inhibits the Epithelial-Mesenchymal Transition of Esophageal Cancer Cells By Twist-Related Protein 1-Mediated Modulation of Melanoma Associated Antigen A4 (MAGEA4)". DOI: 10.3727/096504017 x14972679378357 Because of COVID-19, the lab we worked together was no longer functioning and closed. When reviewing the data of the paper completed in cooperation with the original laboratory, we found that some of the data in the above article were not scientific enough, some Western Blot images were not clear enough (as in FIG 1, the band of α-SMA was blurt and do not seem darker than vimentin but lighter than E-adherin), and some of the research data contained excessive standard errors (as in FIG 2B, standard error of vimentin and α-SMA of miR-539 mimic +Pb-TWIST1(IV) were too large , so the average of the expression may be not accurate), which may lead to the researchers' wrong interpretation of the data and misjudgment of its scientific nature. For the sake of rigor, we took the initiative to contact the experimental operator of the original study. Unfortunately, the person who completed the primary operation of the original study has left China to study in the United States. Due to COVID-19 and other reasons, we could not contact this experimenter to confirm the original research data, so we cannot repeat and verify the data for the time being. As the corresponding author, after found the problem, I contacted Dr. Zhili Cao and Xiang Zheng, and the other author, Dr. Lei Cao at the first time. I told them all the thing we found above. After careful discussion, all the author agreed that, based on the need of scientific, rigor, we are deeply sorry to apply to the editorial office for withdraw the paper. My team and I have noticed that your journal has been developing very well in recent years, and its impact factors have been rising all the way. Congratulations to your team! We are very sorry that there may be errors in our interpretation of the data due to our imprecise interpretation, thus affecting the scientific nature of the conclusion of the article. My team and I have complied with the AGREEMENT FOR WITHDRAWAL OF MANUSCRIPT, and have completed the payment of the fee on December 4, 2020, 300$. Please see the attachment for related procedures. We hope your journal would approve our application for retraction of this article. Sincerely Yours, Naixin Liang 2020.12.4

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