ArticleCell cycle (Georgetown, Tex.)2020
Promoting roles of long non-coding RNA FAM83H-AS1 in bladder cancer growth, metastasis, and angiogenesis through the c-Myc-mediated ULK3 upregulation.
Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Bridging autophagy and endolysosomal dysfunction: Role of bridging integrator 1 in Alzheimer's disease.Neural regeneration research · 2026Article
- Unc-51 like kinase 3 induces reticulophagy by mediating the GLI1/CAMK2B signaling pathway to promote the malignant progression of prostate cancer.American journal of cancer research · 2026Article
- The emerging roles and mechanisms of FAM83H‑AS1 in cancer: Pathophysiology and therapeutic implications (Review).Oncology letters · 2025Review
- BIN1 deficiency enhances ULK3-dependent autophagic flux and reduces dendritic size in mouse hippocampal neurons.Autophagy · 2025Article
- ZC3H13 promotes autophagy in bladder cancer through m6A methylation modification of PJA2 and ubiquitination of KSR1.Human cell · 2024Article
- An Overview of Angiogenesis in Bladder Cancer.Current oncology reports · 2023Review
- The crosstalk between long non-coding RNAs and the hedgehog signaling pathway in cancer.Medical oncology (Northwood, London, England) · 2022Review
- LncRNA HEIH/miR-4500/IGF2BP1/c-Myc Feedback Loop Accelerates Bladder Cancer Cell Growth and Stemness.Bladder cancer (Amsterdam, Netherlands) · 2022Article
- Biological functions and clinical significance of long noncoding RNAs in bladder cancer.Cell death discovery · 2021Review
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8 authors.
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Abstract
Long non-coding RNA (lncRNA) FAM83H-AS1 has been recently identified with oncogenic roles in many human cancers. But its role in bladder cancer (BCa) pathogenesis and the mechanisms are largely unstudied. This study aims to evaluate the roles of FAM83H-AS1 in the malignant behaviors and the angiogenesis of BCa cells and the mechanical molecules involved. High expression of FAM83H-AS1 was found in 82 BCa tissues and in BCa cell lines compared to the normal ones. FAM83H-AS1 downregulation in T24 and BK10 cells inhibited viability, colony formation, migration, invasion, and angiogenesis of BCa cells and increased cell apoptosis. FAM83H-AS1 was found to bind to the transcription factor c-Myc to activate ULK3 expression. Overexpression of ULK3 was further introduced into T24 and BK10 cells in the presence of FAM83H-AS1 silencing, which blocked the inhibitory effects of FAM83H-AS1 downregulation on BCa cell growth. The activity of the Hedgehog signaling pathway was suppressed by FAM83H-AS1 while recovered by ULK3. Suppression of the Hedgehog pathway reduced the malignant behaviors of BCa cells promoted by ULK3. The
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