Metastatic EMT Phenotype Is Governed by MicroRNA-200-Mediated Competing Endogenous RNA Networks

Uhan, Sara; Hauptman, Nina

doi:10.3390/cells11010073

Cited by 11 publications

(2 citation statements)

References 164 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In conclusion, our study confirmed that silencing lncRNA PCED1B-AS1 directly regulates miR-3681-3p/MAP2K7 signaling axis and inhibited proliferation, invasion and EMT processes of gastric cancer cell lines. More and more reports have confirmed that non-coding RNAs have complex regulatory networks, that is, multiple downstream target molecules, which regulated disease progression in multiple ways [ 27 ]. Therefore, the downstream molecule of lncRNA PCED1B-AS1 in the progression of gastric cancer needs to be further studied to clarify its specific marker in gastric cancer.…”

Section: Discussionmentioning

confidence: 99%

LncRNA PCED1B-AS1 mediates miR-3681-3p/MAP2K7 axis to promote metastasis, invasion and EMT in gastric cancer

Cao,

Yang,

Duan

et al. 2024

Biol Direct

View full text Add to dashboard Cite

Background LncRNA PCED1B-AS1 is abnormally expressed in multiple cancers and has been confirmed as an oncogene. Our study aimed to investigate the regulatory mechanism of lncRNA PCED1B-AS1 in gastric cancer. Methods TCGA database was used to analyze the abnormal expression of lncRNA PCED1B-AS1 in gastric cancer. By database prediction and mass spectrometric analysis, miR-3681-3p and MAP2K7 are potential downstream target molecules of lncRNA PCED1B-AS1 and verified by dual-luciferase report assay. RT-qPCR analysis and western blot were performed to detect the expressions of PCED1B-AS1 and MAP2K7 in gastric cancer cell lines and tissues. CCK-8 kit was applied to measure the cell viability. Wound healing and Transwell experiment were used to detect the migration and invasion. Western blot and immunohistochemical staining were performed to detect the expressions of EMT-related proteins in tissues. The changes of tumor proliferation were detected by xenograft experiment in nude mice. Results PCED1B-AS1 expression was higher but miR-3681-3 expression was lower in gastric cancer cell lines or tissues, compared to normal group. Function analysis verified PCED1B-AS1 promoted cell proliferation and inhibited cell apoptosis in gastric cancer cells in vitro and in vivo. LncRNA PCED1B-AS1 could bind directly to miR-3681-3p, and MAP2K7 was found to be a downstream target of miR-3681-3p. MiR-3681-3p mimics or si-MAP2K7 could partly reverse the effect of PCED1B-AS1 on gastric cancer cells. Conclusion PCED1B-AS1 accelerated cell proliferation and inhibited cell apoptosis through sponging miR-3681-3p to upregulate MAP2K7 expression in gastric cancer, which indicated PCED1B-AS1/miR-3681-3p/MAP2K7 axis may serve as a potential therapeutic target for gastric cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

LncRNA PCED1B-AS1 mediates miR-3681-3p/MAP2K7 axis to promote metastasis, invasion and EMT in gastric cancer

Cao,

Yang,

Duan

et al. 2024

Biol Direct

View full text Add to dashboard Cite

show abstract

“…The relationship of ceRNAs to outcomes in TNBC is typically a result of the direct effects on disease progression, e.g., metastasis. As discussed previously, ceRNA networks with miR-200 family members as central factors in controlling EMT and metastatic phenotypes in TNBC and other cancers [ 24 , 46 , 95 ]. Specific lncRNAs have been found to affect or predict metastasis of TNBC to specific sites.…”

Section: Significance Of Cernets Alterations In Tnbcmentioning

confidence: 99%

Genomic Alterations Affecting Competitive Endogenous RNAs (ceRNAs) and Regulatory Networks (ceRNETs) with Clinical Implications in Triple-Negative Breast Cancer (TNBC)

Qattan

2024

IJMS

View full text Add to dashboard Cite

The concept of competitive endogenous RNA regulation has brought on a change in the way we think about transcriptional regulation by miRNA–mRNA interactions. Rather than the relatively simple idea of miRNAs negatively regulating mRNA transcripts, mRNAs and other non-coding RNAs can regulate miRNAs and, therefore, broad networks of gene products through competitive interactions. While this concept is not new, its significant roles in and implications on cancer have just recently come to light. The field is now ripe for the extrapolation of technologies with a substantial clinical impact on cancer. With the majority of the genome consisting of non-coding regions encoding regulatory RNAs, genomic alterations in cancer have considerable effects on these networks that have been previously unappreciated. Triple-negative breast cancer (TNBC) is characterized by high mutational burden, genomic instability and heterogeneity, making this aggressive breast cancer subtype particularly relevant to these changes. In the past few years, much has been learned about the roles of competitive endogenous RNA network regulation in tumorigenesis, disease progression and drug response in triple-negative breast cancer. In this review, we present a comprehensive view of the new knowledge and future perspectives on competitive endogenous RNA networks affected by genomic alterations in triple-negative breast cancer. An overview of the competitive endogenous RNA (ceRNA) hypothesis and its bearing on cellular function and disease is provided, followed by a thorough review of the literature surrounding key competitive endogenous RNAs in triple-negative breast cancer, the genomic alterations affecting them, key disease-relevant molecular and functional pathways regulated by them and the clinical implications and significance of their dysregulation. New knowledge of the roles of these regulatory mechanisms and the current acceleration of research in the field promises to generate insights into the diagnosis, classification and treatment of triple-negative breast cancer through the elucidation of new molecular mechanisms, therapeutic targets and biomarkers.

show abstract

Mesenchymal Stem Cells, Cancer Stem Cells (CSCs), and Circulating Tumor Cells (CTCs): Roles and Combinations in Tumor Growth and Dissemination

Aramini,

Masciale,

Banchelli

et al. 2023

Handbook of Stem Cell Applications

View full text Add to dashboard Cite

Metastatic EMT Phenotype Is Governed by MicroRNA-200-Mediated Competing Endogenous RNA Networks

Cited by 11 publications

References 164 publications

LncRNA PCED1B-AS1 mediates miR-3681-3p/MAP2K7 axis to promote metastasis, invasion and EMT in gastric cancer

LncRNA PCED1B-AS1 mediates miR-3681-3p/MAP2K7 axis to promote metastasis, invasion and EMT in gastric cancer

Genomic Alterations Affecting Competitive Endogenous RNAs (ceRNAs) and Regulatory Networks (ceRNETs) with Clinical Implications in Triple-Negative Breast Cancer (TNBC)

Mesenchymal Stem Cells, Cancer Stem Cells (CSCs), and Circulating Tumor Cells (CTCs): Roles and Combinations in Tumor Growth and Dissemination

Contact Info

Product

Resources

About