MicroRNA‑214 promotes the EMT process in melanoma by downregulating CADM1 expression

Wang, Shujun; Li, Weiwei; Wen, Cong‐Ji; Diao, Yong; Zhao, Tianlan

doi:10.3892/mmr.2020.11446

Cited by 10 publications

(6 citation statements)

References 47 publications

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“…After culturing at 37°C for 24 h, cells on the underside of the membrane were fixed with 5% glutaraldehyde for 30 min at 4°C, and then stained with 0.5% crystal violet for 30 min at room temperature. Images were taken using an inverted light microscope (Leica, Germany) and invading cells in different areas were counted and analyzed using ImageJ software [ 29 ]. All experiments were repeated three times.…”

Section: Methodsmentioning

confidence: 99%

CMaf-Inducing Protein Promotes LUAD Proliferation and Metastasis by Activating the MAPK/ERK Pathway

Wang²,

Qian

2022

Evidence-Based Complementary and Alternative Medicine

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Objective. Previous studies have shown that cMaf-inducing protein (CMIP) promotes tumorigenesis and progression, however, the role of CMIP in lung adenocarcinoma (LUAD) and its molecular mechanism remain unclear. Methods. In this study, the Human Protein Atlas and Kaplan–Meier Plotter database were used to analyze the expression and prognostic value of CMIP in LUAD. Then, the expression levels of CMIP in LUAD tissues and cells were detected by qRT-PCR and western blot. The lentiviral vector was used to establish a stable transfected cell line, and the transfection efficiency was detected by qRT-PCR. MTT assay, colony formation assay, transwell assay, and wound healing assay were used to evaluate the function of CMIP in LUAD. In addition, the effect of CMIP on the MAPK/ERK pathway in LUAD cells was analyzed by western blot. Results. The expression level of CMIP was significantly increased in LUAD cell and tissue samples, and the high expression of CMIP was associated with overall survival (OS) and progression-free survival (PFS) in LUAD patients. In vitro experiments showed that CMIP overexpression significantly promoted the proliferation, migration, and invasion of A549 cells. CMIP knockout significantly inhibited the proliferation, migration, and invasion of H1299 cells. In addition, it was observed that the expression levels of the MAPK/ERK pathway-related proteins were significantly increased in CMIP-overexpressed A549 cells, and promoted cell proliferation, migration, and invasion, while U0126 could significantly reverse the activation of the MAPK/ERK pathway by CMIP overexpression, and inhibit the proliferation, migration, and invasion of A549 cells. Conclusion. Our study shows that CMIP, as an oncogene, is associated with poor patient prognosis, and may promote the proliferation and metastasis of LUAD by activating the MAPK/ERK pathway. Therefore, CMIP may be a new potential therapeutic target for LUAD.

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Section: Methodsmentioning

confidence: 99%

CMaf-Inducing Protein Promotes LUAD Proliferation and Metastasis by Activating the MAPK/ERK Pathway

Wang²,

Qian

2022

Evidence-Based Complementary and Alternative Medicine

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“…In melanoma, another miRNA molecule, miR-214, is prometastatic. MiR-214 silences cell adhesion molecule 1 (CADM1), a known tumor suppressor, thus leading to higher migration and invasion of melanoma cells and EMT promotion, in which miR-214 contributes to annoikis resistance and subsequently to extravasation [ 99 , 100 ]. The relevance of the miR-199/miR-214 cluster was also described in triple negative breast carcinoma (TNBC); however, in TNBC, the overexpression of miRNAs from the miR-199/miR-214 cluster leads to the inhibition of EMT, higher expression of epithelial markers E-cadherin and β-catenin, and decreased expression of the mesenchymal marker SNAIL2 (also known as SLUG) [ 101 ].…”

Section: Micrornas Involved In the Metastatic Cascadementioning

confidence: 99%

The Significance of MicroRNAs in the Molecular Pathology of Brain Metastases

Siegl

Večeřa

Roskova

et al. 2022

Cancers

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Brain metastases are the most frequent intracranial tumors in adults and the cause of death in almost one-fourth of cases. The incidence of brain metastases is steadily increasing. The main reason for this increase could be the introduction of new and more efficient therapeutic strategies that lead to longer survival but, at the same time, cause a higher risk of brain parenchyma infiltration. In addition, the advances in imaging methodology, which provide earlier identification of brain metastases, may also be a reason for the higher recorded number of patients with these tumors. Metastasis is a complex biological process that is still largely unexplored, influenced by many factors and involving many molecules. A deeper understanding of the process will allow the discovery of more effective diagnostic and therapeutic approaches that could improve the quality and length of patient survival. Recent studies have shown that microRNAs (miRNAs) are essential molecules that are involved in specific steps of the metastatic cascade. MiRNAs are endogenously expressed small non-coding RNAs that act as post-transcriptional regulators of gene expression and thus regulate most cellular processes. The dysregulation of these molecules has been implicated in many cancers, including brain metastases. Therefore, miRNAs represent promising diagnostic molecules and therapeutic targets in brain metastases. This review summarizes the current knowledge on the importance of miRNAs in brain metastasis, focusing on their involvement in the metastatic cascade and their potential clinical implications.

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“…Wei et al [8] showed that RNF128 affects the EMT process of melanoma by acting on the ubiquitination of CD44 and CTTN in melanoma cells through the Wnt/β-catenin signaling pathway. Wang et al [31] showed that microRNA-214 downregulated CADM1 in melanoma cells, thereby promoting EMT progression in melanoma. Together, these results suggest that the development of melanoma may be favored by the promotion of cellular EMT.…”

Section: It Has Been Reported Previously Thatmentioning

confidence: 99%

Exosomal miR-22-3p from Mesenchymal Stem Cells Inhibits the Epithelial-Mesenchymal Transition (EMT) of Melanoma Cells by Regulating LGALS1

Chen¹,

Fang²,

Li³

et al. 2022

Front. Biosci. (Landmark Ed)

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Background:The mortality rate from melanoma has been rising and hence new therapeutic approaches for this disease have received extensive attention, especially the search for novel therapeutic targets. The aim of this study was to find new targets for the treatment of melanoma through a bioinformatics and experimental approach. Methods: First, we screened for differentially expressed genes (DEGs) and differentially expressed miRNAs (DEMs) between melanoma and normal tissues using the TCGA-SKCM, GTEX, and GSE24996 datasets. Next, we identified epithelial-mesenchymal transition (EMT)-related DEGs and analyzed their expression levels and association with patient survival. The expression level of DEGs was then confirmed in normal human melanocytes and melanoma cells. Bioinformatics analysis was used to identify miRNAs that targeted the most highly expressed DEG, LGALS1, and their binding confirmed using dual luciferase. Enriched pathways for the LGALS1 target miR-22-3p were also analyzed. miR-22-3p was overexpressed in cells in order to investigate changes in cell activity and in related genes and proteins. Exosomes from human bone marrow mesenchymal stem cells (MSCs) were coated with miR-22-3p to examine its effect on EMT. Results: The expression levels of LGALS1, CPXM1, and APLNR were higher in melanoma than in normal tissues and were associated with worse patient survival. The differential expression of these genes was confirmed using normal human skin melanocytes (PIG1) and human melanoma cells (WM-266-4). LGALS1 was the most differentially expressed gene between WM-266-4 and PIG1 cells, and was also predicted to be a target for miR-22-3p. The results of dual luciferase experiments confirmed that miR-22-3p could bind to LGALS1. Following the overexpression of miR-22-3p in WM-266-4 cells, the cell viability decreased, the expression levels of LGALS1, VIM and SNAI2 decreased, the expression level of CDH1 increased, and cell apoptosis increased. Transfection of miR-22-3p using exosomes resulted in similar effects. Conclusions: We identified three genes (LGALS1, CPXM1, APLNR) that showed a high level of differential expression in melanoma. LGALS1 is a target for miR-22-3p binding and this can inhibit the EMT of melanoma cells, thereby preventing the development of melanoma. Moreover, exosomes secreted by MSCs can be loaded with miR-22-3p, thus regulating the EMT process in melanoma cells.

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MicroRNA‑214 promotes the EMT process in melanoma by downregulating CADM1 expression

Cited by 10 publications

References 47 publications

CMaf-Inducing Protein Promotes LUAD Proliferation and Metastasis by Activating the MAPK/ERK Pathway

CMaf-Inducing Protein Promotes LUAD Proliferation and Metastasis by Activating the MAPK/ERK Pathway

The Significance of MicroRNAs in the Molecular Pathology of Brain Metastases

Exosomal miR-22-3p from Mesenchymal Stem Cells Inhibits the Epithelial-Mesenchymal Transition (EMT) of Melanoma Cells by Regulating LGALS1

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