ArticleCancer gene therapy2021
Tumor-suppressive microRNA-551b-3p targets H6PD to inhibit gallbladder cancer progression.
Article in Cancer gene therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Deciphering the YY1/ lncRNA BLACAT1/miR-605-3p axis in glioblastoma: implications for therapy.NPJ precision oncology · 2025Article
- RNAa: Mechanisms, therapeutic potential, and clinical progress.Molecular therapy. Nucleic acids · 2025Review
- MicroRNA Profiling in Papillary Thyroid Cancer.International journal of molecular sciences · 2024Article
- Recent Advances in Extracellular Vesicles in Amyotrophic Lateral Sclerosis and Emergent Perspectives.Cells · 2023Review
- Article
- Elevated Hexose-6-Phosphate Dehydrogenase Regulated by OSMR-AS1/hsa-miR-516b-5p Axis Correlates with Poor Prognosis and Dendritic Cells Infiltration of Glioblastoma.Brain sciences · 2022Article
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gallbladder cancer (GBC) is a highly malignant cancer with poor prognosis. Extensive studies have reported the vital functionality of several microRNAs (miRNAs) in numerous human cancers, including GBC. Microarray analysis has identified the differentially expressed miR-551b-3p in GBC. Therefore, this study aims to validate the underlying mechanism by which miR-551b-3p participated in epithelial-mesenchymal transition (EMT), invasion and migration of GBCs. Bioinformatic analysis predicted the binding of miR-551b-3p to H6PD. We validated the reduced miR-551b-3p expression and increased H6PD expression in the GBC tissues and GBC cell lines. Artificial modulation of miR-551b-3p and H6PD (down- and upregulation) was conducted to explore their roles in EMT, invasive, and migratory abilities of GBCs, and the tumor-bearing mice were used to determine tumor growth. Overexpression of miR-551b-3p or silencing of H6PD was observed to suppress the expressions of N-cadherin and vimentin, and to promote the expression of E-cadherin, along with reduced invasive and migratory ability of GBCs. Mechanistically, miR-551b-3p could evidently target and inhibit the expression of H6PD. Moreover, in vivo experiments substantiated the tumor-inhibiting activities of miR-551b-3p in nude mice. Conjointly, our study suggests that overexpression of miR-551b-3p inhibited the EMT, migration, and invasion of GBCs by inhibiting the expression of H6PD, indicating that miR-551b-3p may serve as a potential target for future development of therapeutic strategies for GBC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.