Crosstalk between miR‐215 and epithelial‐mesenchymal transition specific markers (E‐cadherin and N‐cadherin) in different stages of chronic HCV Infection

Omran, Nermeen M.; El-Sherbini, Sherif M.; Hegazy, Osama; El-Shaarawy, Ahmed Ahmed; Talaat, Roba M.

doi:10.1002/jmv.25637

Cited by 8 publications

(9 citation statements)

References 59 publications

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“…EMT is induced via various alterations, including loss of basal apical polarity, cell adhesion and gain of motility [41]. E-cadherin levels have been found to have decreased during EMT, whereas N-cadherin expression was elevated, resulting in a cadherin switch [42]. miR-1 expression could restore E-cadherin expression in order to increase cell-cell contacts through the formation of adherent junctions [43,44].…”

Section: Discussionmentioning

confidence: 99%

Downregulation of miR-1 in colorectal cancer promotes radioresistance and aggressive phenotypes

Wu¹,

Pu²,

Su³

et al. 2020

J. Cancer

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Background: Colorectal cancer (CRC) remains to be one of the most common malignancies worldwide. Various studies have demonstrated that microRNAs (miRs) play a critical role in regulating cancer progression and sensitivity to chemoradiotherapy. miR-1 was found to be aberrantly expressed in CRC. However, it has not been fully elucidated whether miR-1 regulated CRC cell radioresistance. Methods: The expression of miR-1 was detected using quantitative real-time polymerase chain reaction in CRC tissues and cell lines. Colony survival and proliferation were determined using colony formation assay and MTT assay, respectively. Apoptosis and levels of related proteins, Bax and Bcl-2, were detected using flow cytometer assay and western blotting analysis. Migration and invasion were measured using wound healing assay and transwell invasion assay. The levels of invasion-associated proteins, E-cadherin, MMP2 and MMP9, were detected using western blotting analysis. Results: miR-1 was found to be downregulated in CRC tissues and cell lines compared with adjacent normal tissues. In vitro, miR-1 overexpression significantly suppressed colony survival and proliferation, and induced cell apoptosis under irradiation, but no apoptosis was detected without irradiation. Furthermore, miR-1 mimics promoted the expression of Bax and E-cadherin and decreased the expression of Bcl-2, MMP2 and MMP9, and apparently impaired the invasion and migration of CRC cells in synergy with radiotherapy. Conclusion: miR-1 enhanced the radiosensitivity of CRC cells by inducing cell apoptosis and the synergic inhibition of aggressive phenotypes, which may serve as a promising therapeutic target for CRC patients.

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Section: Discussionmentioning

confidence: 99%

Downregulation of miR-1 in colorectal cancer promotes radioresistance and aggressive phenotypes

Wu¹,

Pu²,

Su³

et al. 2020

J. Cancer

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“…These miRNAs are well associated with other viral scenarios such as hepatitis C, hepatitis B, influenza, tuberculosis, etc. [ 22 , 23 , 24 , 25 , 26 , 27 , 28 ], but our study is the first report of them being associated in RV infection.…”

Section: Discussionmentioning

confidence: 64%

Rotavirus-Mediated Suppression of miRNA-192 Family and miRNA-181a Activates Wnt/β-Catenin Signaling Pathway: An In Vitro Study

Banerjee

Chawla‐Sarkar

Mukherjee

2022

Viruses

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The significance of the Wnt/β-catenin signaling cascade in Rotavirus (RV) infection has not been elucidated. In this study, we attempt to elucidate the importance of the Wnt/β-catenin pathway in the RV pathogenesis and investigate a miRNA-mediated approach to regulate the pathway to repress the RV infection in the host. The regulation of the Wnt signaling pathway in terms of β-catenin accumulation and activation was analyzed by Western blotting and Confocal imaging analysis. The expression levels of miR-192 family members and miR-181a were enquired into using qPCR assays, whereas their targets in the Wnt pathway were confirmed using the Luciferase Reporter Assays. Members of the miR-192 family and miR-181a, which target the components of the pathway, were also found to be considerably decreased in expression during RV infection. Ectopic expression of these miRNAs could restrict the RV pathogenesis by targeting the intermediates of the Wnt signaling pathway. The miR-192 family and miR-181a were capable of suppressing the RV infection via targeting of the Wnt/β-catenin pathway. The study not only highlights the role of the Wnt signaling cascade in RV infection but also suggests that miRNAs can synergistically decrease RV replication by a significant amount. Thus, the miR-192 family and miR-181a present themselves as prospective antivirals against RV infection.

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“…The gender disparity in HCC incidence suggests that approximately 2-8 times as many men develop HCC than women, which may result from the association of sex hormones with the progression of HBV-induced HCC [ 3 , 4 ]. Tumor metastasis is usually coupled with the aggravation of liver cancer and higher mortality of HCC patients [ 5 ]. In addition, deregulated cell proliferation combined with suppressed apoptosis constitutes the minimal common form upon which all neoplastic evolution occurs [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

Identification of alanine aminotransferase 1 interaction network via iTRAQ-based proteomics in alternating migration, invasion, proliferation and apoptosis of HepG2 cells

Zhang

et al. 2022

Aging

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Objective: To investigate the mechanism of alanine aminotransferase 1 (ALT1) in the progression of HCC, the differentially expressed proteins (DEPs) in the ALT1 interaction network were identified by targeted proteomic analysis. Methods: Wound healing and transwell assays were conducted to assess the effect of ALT1 on cellular migration and invasion. Cell Counting Kit-8 (CCK-8), colony formation, and flow cytometry assays were performed to identify alterations in proliferation and apoptosis. After coimmunoprecipitation processing, mass spectrometry with iso-baric tags for relative and absolute quantitation was utilized to explore the protein interactions in ALT1 knockdown HepG2 cells. Results: The results showed that ALT1 knockdown inhibits the migration, invasion, proliferation of HepG2 cells, and promotes apoptosis. A total of 116 DEPs were identified and the bioinformatics analysis suggested that the ALT1-interacting proteins were primarily associated with cellular and metabolic processes. Knockdown of ALT1 in HepG2 cells reduced the expression of Ki67 and epithelial cell adhesion molecule (EP-CAM), while the expression of apoptosis-stimulating protein 2 of p53 (ASPP2) was increased significantly. Suppression of the ALT1 and EP-CAM expression contributed to alterations in epithelial-mesenchymal transition (EMT) -associated markers and matrix metalloproteinases (MMPs). Additionally, inhibition of ALT1 and Ki67 also decreased the expression of apoptosis and proliferation factors. Furthermore, inhibition of ALT1 and ASPP2 also changed the expression of P53, which may be the signaling pathway by which ALT regulates these biological behaviors. Conclusions: This study indicated that the ALT1 protein interaction network is associated with the biological behaviors of HepG2 cells via the p53 signaling pathway.

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Crosstalk between miR‐215 and epithelial‐mesenchymal transition specific markers (E‐cadherin and N‐cadherin) in different stages of chronic HCV Infection

Cited by 8 publications

References 59 publications

Downregulation of miR-1 in colorectal cancer promotes radioresistance and aggressive phenotypes

Downregulation of miR-1 in colorectal cancer promotes radioresistance and aggressive phenotypes

Rotavirus-Mediated Suppression of miRNA-192 Family and miRNA-181a Activates Wnt/β-Catenin Signaling Pathway: An In Vitro Study

Identification of alanine aminotransferase 1 interaction network via iTRAQ-based proteomics in alternating migration, invasion, proliferation and apoptosis of HepG2 cells

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