PADI4 modulates the invasion and migration of osteosarcoma cells by down-regulation of epithelial-mesenchymal transition

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.

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MicroRNA‐4429 restrains colorectal cancer cell invasion and migration via regulating SMAD3‐induced epithelial–mesenchymal transition

Journal of Cellular Physiology ◽

10.1002/jcp.30271 ◽

2021 ◽

Author(s):

Hongwen Li ◽

Weijie Liang ◽

Hongyu Zhang ◽

Yifang Shui ◽

Zhe Zhang

Keyword(s):

Colorectal Cancer ◽

Cancer Cell ◽

Cell Invasion ◽

Epithelial Mesenchymal Transition ◽

Colorectal Cancer Cell ◽

Cancer Cell Invasion ◽

Mesenchymal Transition ◽

Invasion And Migration ◽

And Migration

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Benzotriazole Enhances Cell Invasive Potency in Endometrial Carcinoma Through CTBP1-Mediated Epithelial-Mesenchymal Transition

Cellular Physiology and Biochemistry ◽

10.1159/000486123 ◽

2017 ◽

Vol 44 (6) ◽

pp. 2357-2367 ◽

Cited By ~ 3

Author(s):

Yiquan Wang ◽

Chencheng Dai ◽

Cheng Zhou ◽

Wenqu Li ◽

Yujia Qian ◽

...

Keyword(s):

Endometrial Carcinoma ◽

Epithelial Mesenchymal Transition ◽

Expression Patterns ◽

Underlying Mechanism ◽

Carcinoma Cells ◽

Mesenchymal Transition ◽

Invasion And Migration ◽

Female Reproductive Health ◽

Gene Microarray Analysis ◽

And Migration

Background/Aims: Benzotriazole (BTR) and its derivatives, such as intermediates and UV stabilizers, are important man-made organic chemicals found in everyday life that have been recently identified as environmental toxins and a threat to female reproductive health. Previous studies have shown that BTR could act as a carcinogen by mimicking estrogen. Environmental estrogen mimics could promote the initiation and development of female cancers, such as endometrial carcinoma, a type of estrogenic-sensitive malignancy. However, there is little information on the relationship between BTR and endometrial carcinoma. In this study, we aimed to demonstrate the biological function of BTR in endometrial carcinoma and explored the underlying mechanism. Methods: The CCK-8 assay was performed to detect cell viability; transwell-filter assay was used to assess cell invasion; gene microarray analysis was employed to determine gene expression patterns in response to BTR treatment; western blotting and quantitative reverse transcription polymerase chain reaction (qRT-PCR) were carried out to detect the expression levels of BTR-related genes. Results: Our data showed that BTR could induce the invasion and migration of endometrial carcinoma cells (Ishikawa and HEC-1-B). In addition, BTR increased the expression level of CTBP1, which could enhance the epithelial-mesenchymal transition (EMT) in cancer cells. Moreover, CTBP1 silencing reversed the effect of BTR on EMT progression in endometrial carcinoma cells. Conclusion: This study indicates that BTR could act as a carcinogen to promote the development of endometrial carcinoma mainly through CTBP1-mediated EMT, which deserves more attention.

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BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

Virology Journal ◽

10.1186/s12985-020-01399-7 ◽

2020 ◽

Vol 17 (1) ◽

Cited By ~ 2

Author(s):

Yigang Zeng ◽

Jiajia Sun ◽

Juan Bao ◽

Tongyu Zhu

Keyword(s):

Bladder Cancer ◽

Signaling Pathway ◽

Epithelial Mesenchymal Transition ◽

Cell Model ◽

Mesenchymal Transition ◽

Invasion And Migration ◽

Urothelial Carcinomas ◽

Bk Polyomavirus ◽

And Migration

Abstract Background Recent studies have confirmed the integration of the BK polyomavirus (BKPyV) gene into the cellular genome of urothelial carcinomas in transplant recipients, further confirming the correlation between BKPyV and urothelial carcinomas after transplantation. However, the role BKPyV infections play in the biological function of bladder cancer remains unclear. Methods We developed a BKPyV-infected bladder cancer cell model and a mice tumor model to discuss the role of BKPyV infections. Results Our research proves that BKPyV infections promote the proliferation, invasion and migration of bladder cancer cells, while the activation of β-catenin signaling pathway is one of its mediation mechanisms. Conclusions We first described BKPyV infection promotes the proliferation, invasion and migration of bladder cancer. We verified the role of β-catenin signaling pathway and Epithelial-Mesenchymal Transition effect in BKPyV-infected bladder cancer. These results provide meaningful information towards the diagnosis and treatment of clinical bladder cancer.

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