Chondroitin polymerizing factor promotes breast carcinoma cell proliferation, invasion and migration and affects expression of epithelial‐mesenchymal transition‐related markers

Background/Aims: Epithelial-mesenchymal transition (EMT) is recognized as a crucial mechanism in breast cancer progression and metastasis. Paired-related homeobox 2 (Prrx2) has been identified as a new EMT inducer in cancer, but the underlying mechanisms are still poorly understood. Methods: The expression of Prrx2 was assessed by immunohistochemistry in breast cancer tissues to evaluate the clinicopathological significance of Prrx2, as well as the correlation between Prrx2 and EMT. Short hairpin RNA knockdown of Prrx2 was used to examine cellular effects of Prrx2, detecte the expression of Wnt/β-catenin signaling and EMT-associated proteins, and observe cell proliferation, invasion and migration abilities in vitro and in vivo. Results: Clinical association studies showed that Prrx2 expression was related to tumor size, lymph node metastasis, tumor node metastasis stages, EMT and poor survival. Results also showed that knockdown of Prrx2 could alter cell morphology, suppressed the abilities of cell proliferation, invasion and migration in breast cancer. Moreover, silencing of Prrx2 induced the mesenchymal-epithelial transition and prevented nuclear translocation of β-catenin, inhibited wnt/β-catenin signaling pathway. Conclusion: Our study indicated that Prrx2 may be an important activator of EMT in human breast cancer and it can serve as a molecular target of therapeutic interventions for breast cancer.

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LncRNA, CRNDE promotes osteosarcoma cell proliferation, invasion and migration by regulating Notch1 signaling and epithelial-mesenchymal transition

Experimental and Molecular Pathology ◽

10.1016/j.yexmp.2017.12.002 ◽

2018 ◽

Vol 104 (1) ◽

pp. 19-25 ◽

Cited By ~ 25

Author(s):

Zheng Li ◽

Yonghua Tang ◽

Wujun Xing ◽

Wei Dong ◽

Zhichou Wang

Keyword(s):

Cell Proliferation ◽

Epithelial Mesenchymal Transition ◽

Osteosarcoma Cell ◽

Mesenchymal Transition ◽

Invasion And Migration ◽

Notch1 Signaling ◽

And Migration

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SDC1 knockdown induces epithelial–mesenchymal transition and invasion of gallbladder cancer cells via the ERK/Snail pathway

Journal of International Medical Research ◽

10.1177/0300060520947883 ◽

2020 ◽

Vol 48 (8) ◽

pp. 030006052094788

Author(s):

Zixiang Liu ◽

Hao Jin ◽

Song Yang ◽

Haiming Cao ◽

Ziyan Zhang ◽

...

Keyword(s):

Cell Proliferation ◽

Gallbladder Cancer ◽

Epithelial Mesenchymal Transition ◽

Negative Control ◽

Cell Counting ◽

Mesenchymal Transition ◽

Expression Levels ◽

Invasion And Migration ◽

And Migration ◽

E Cadherin

Background Expression levels of the cell adhesion molecule syndecan-1 (SDC1) have been shown to be inversely proportional to tumor differentiation and prognosis. However, its role in the development of gallbladder cancer (GBC) remains unclear. Methods We knocked down SDC1 in GBC cells by RNA interference and determined its roles in cell proliferation, apoptosis, invasion, and migration by Cell Counting Kit-8, colony-formation, flow cytometry, Hoechst 33342 staining, transwell invasion, and scratch wound assays. Expression levels of epithelial–mesenchymal transition (EMT)-related and extracellular signal-regulated kinase (ERK)/Snail pathway proteins were determined by western blotting and immunofluorescence. Results Cell proliferation, invasion, and migration were all increased in GBC cells with SDC1 knockdown, compared with cells in the blank control and negative control groups, but apoptosis was similar in all three groups. E-cadherin and β-catenin expression levels were significantly lower and N-cadherin, vimentin, p-ERK1/2, and Snail expression were significantly higher in the SDC1 knockdown group compared with both controls, while ERK1/2 levels were similar in all groups. Reduced E-cadherin and increased vimentin levels were confirmed by immunofluorescence. Conclusions SDC1 knockdown promotes the proliferation, invasion, and migration of GBC cells, possibly by regulating ERK/Snail signaling and inducing EMT and cancer cell invasion.

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The Pseudogene DUXAP8 Promotes Colorectal Cancer Cell Proliferation, Invasion, and Migration by Inducing Epithelial-Mesenchymal Transition Through Interacting with EZH2 and H3K27me3

OncoTargets and Therapy ◽

10.2147/ott.s235643 ◽

2020 ◽

Vol Volume 13 ◽

pp. 11059-11070

Author(s):

Wenjing He ◽

Yi Yu ◽

Wei Huang ◽

Guoliang Feng ◽

Junhe Li

Keyword(s):

Colorectal Cancer ◽

Cell Proliferation ◽

Cancer Cell ◽

Epithelial Mesenchymal Transition ◽

Colorectal Cancer Cell ◽

Cancer Cell Proliferation ◽

Mesenchymal Transition ◽

Invasion And Migration ◽

And Migration

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High STRN Expression Promotes HCC Invasion and Migration but Not Cell Proliferation or Apoptosis through Facilitating Epithelial-Mesenchymal Transition

BioMed Research International ◽

10.1155/2020/6152925 ◽

2020 ◽

Vol 2020 ◽

pp. 1-10

Author(s):

Qian-yu Du ◽

Jing-hao Yao ◽

Yong-chun Zhou ◽

Ling-jie Xu ◽

Fu-you Zhao ◽

...

Keyword(s):

Cell Proliferation ◽

Cell Invasion ◽

Tumour Cell ◽

Epithelial Mesenchymal Transition ◽

Morphological Changes ◽

Mesenchymal Transition ◽

Invasion And Migration ◽

Huh7 Cells ◽

And Migration ◽

E Cadherin

A STRN-ALK fusion protein has been recently identified as a potential therapeutic target in multiple cancers; however, the role of STRN alone in regulating the biological function of hepatocellular carcinoma (HCC) remains unclear. In this study, we firstly detected an overexpression of STRN in HCC tissues compared to that in adjacent nontumour (ANT) tissues through IHC analysis, and the expression level of this protein was positively correlated with lymph node metastasis and TNM stage. In vitro, high expression of STRN was also confirmed in different HCC cell lines, and regulation of STRN expression in Huh7 cells did not significantly affect tumour cell proliferation or apoptosis but was positively correlated with tumour cell invasion and migration capacities. Moreover, both the knockdown and overexpression of STRN in Huh7 cells can lead to cell morphological changes that are accompanied with an alteration of epithelial-mesenchymal transition (EMT) molecular markers E-cadherin and Vimentin. Finally, STRN was further proved to be negatively related to E-cadherin expression but positively related to Vimentin expression in human HCC tissue samples. Taken together, STRN is upregulated in HCC and acts as a tumour promoter regulating cell invasion and migration through facilitating the EMT process.

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

Technology in Cancer Research & Treatment ◽

10.1177/15330338211033077 ◽

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.

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