ArticleCancer science2020
FNDC3B 3'-UTR shortening escapes from microRNA-mediated gene repression and promotes nasopharyngeal carcinoma progression.
Article in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 53 citations in OpenAlex.
- Alternative Polyadenylation Drives Runaway Pro-Inflammatory Macrophages in Periodontitis by Enabling Escape From miRNA Repression.Cell proliferation · 2026Article
- APAdeg enhances differentially expressed gene inference by leveraging site-specific signals in APA-seq data.Briefings in bioinformatics · 2026Article
- RPSLearner: A Novel Approach Based on Random Projection and Deep Stacking Learning for Categorizing Non-Small Cell Lung Cancer.Advanced intelligent systems (Weinheim an der Bergstrasse, Germany) · 2026Article
- Exploring the common ferroptosis-related genes and molecular mechanisms in periodontitis and systemic sclerosis via integrated bioinformatics and experimental analysis.Frontiers in cell and developmental biology · 2026Article
- Integrated bioinformatics analysis of common molecular mechanisms and biomarkers in oral squamous cell carcinoma and periodontal disease.Discover oncology · 2025Article
- FNDC3B promotes gastric cancer metastasis via interacting with FAM83H and preventing its proteasomal degradation.Cellular & molecular biology letters · 2025Article
- Non-Muscle Myosin II A: Friend or Foe in Cancer?International journal of molecular sciences · 2024Review
- Unveiling the enigmatic role of MYH9 in tumor biology: a comprehensive review.Cell communication and signaling : CCS · 2024Review
- Identification of fibronectin type III domain containing 3B as a potential prognostic and therapeutic target for pancreatic cancer: a preliminary analysis.European journal of medical research · 2024Article
- Article
- A RBM47 and IGF2BP1 mediated circular FNDC3B-FNDC3B mRNA imbalance is involved in the malignant processes of osteosarcoma.Cancer cell international · 2023Article
- LncRNA SNHG1 promotes nasopharyngeal carcinoma development via targeting miR-424-5p.Histology and histopathology · 2023Article
- circFNDC3B Accelerates Vasculature Formation and Metastasis in Oral Squamous Cell Carcinoma.Cancer research · 2023Article
- Article
- Relationship between NUDT21 mediated alternative polyadenylation process and tumor.Frontiers in oncology · 2023Review
- Non-coding RNAs and epithelial mesenchymal transition in cancer: molecular mechanisms and clinical implications.Journal of experimental & clinical cancer research : CR · 2022Review
- Salidroside suppresses the activation of nasopharyngeal carcinoma cells via targeting miR-4262/GRP78 axis.Cell cycle (Georgetown, Tex.) · 2022Article
- MCL1 alternative polyadenylation is essential for cell survival and mitochondria morphology.Cellular and molecular life sciences : CMLS · 2022Article
- Circ_0006948 Contributes to Cell Growth, Migration, Invasion and Epithelial-Mesenchymal Transition in Esophageal Carcinoma.Digestive diseases and sciences · 2022Article
- Evaluation of ABCA1 and FNDC3B Gene Polymorphisms Associated With Pseudoexfoliation Glaucoma and Primary Angle-Closure Glaucoma in a Saudi Cohort.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Alternative polyadenylation (APA), which induces shortening of the 3'-UTR, is emerging as an important feature in cancer development and progression. Nevertheless, the effects and mechanisms of APA-induced 3'-UTR shortening in nasopharyngeal carcinoma (NPC) remain largely unclear. Fibronectin type III domain containing 3B (FNDC3B) tended to use proximal polyadenylation site and produce shorter 3'-UTR according to our previous sequencing study. Herein, we found that FNDC3B with shorter 3'-UTR could escape from miRNA-mediated gene repression, and caused its increased expression in NPC. Knocking down of FNDC3B inhibited NPC cell proliferation, migration, invasion, and metastasis in vitro and in vivo. Overexpression of FNDC3B, especially those with shorter 3'-UTR, promoted NPC progression. Furthermore, the mechanism study revealed that FNDC3B could bind to and stabilize myosin heavy chain 9 (MYH9) to activate the Wnt/β-catenin signaling pathway. In addition, MYH9 could reverse the inhibitory effects of FNDC3B knockdown in NPC. Altogether, our results suggested that the 3'-UTR shortening of FNDC3B mRNA mediated its overexpression in NPC and promoted NPC progression by targeting MYH9. This newly identified FNDC3B-MYH9-Wnt/β-catenin axis could represent potential targets for individualized treatment in NPC.
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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.