LncRNA FBXL19-AS1 regulates the miR-650/ITGB3 axis to drive pathological progression in Alzheimer's Disease.
4 affiliations
- 1Rongjun Rehabilitation Department 5, Hebei Third Rongjun Youfu Hospital, Baoding, 071000, China.
- 2Department of Neurology III, Taiyuan People's Hospital, Taiyuan, 030025, China.
- 3Neurosurgery Ward 2, Affiliated Hospital of Zunyi Medical University, No. 149, Dalian Road, Huichuan District, Zunyi, 563000, China. [email protected].
- 4Department of Neurosurgery, The First Hospital of Jiaxing, No. 1882, Zhonghuan South Road, Jiaxing, 314001, China. [email protected].
Abstract
Background
Alzheimer's Disease (AD) is a progressive neurodegenerative disorder characterized by complex and not yet fully understood pathological mechanisms. This study was designed to explore the molecular mechanisms of long non-coding RNA (lncRNA) FBXL19-AS1 in the pathological progression of AD.Methods
110 AD patients and 110 healthy controls were recruited for this study. Relevant gene expression was measured using reverse transcription quantitative real-time PCR (RT-qPCR), and the diagnostic performance was assessed through receiver operating characteristic (ROC) curve analysis. AD cell models were established by treating SH-SY5Y and BV2 cells with amyloid β (Aβ)25-35. Cell proliferation was evaluated using the cell counting kit-8 (CCK-8) assay, cell apoptosis was analyzed by flow cytometry, and the secretion levels of inflammatory factors were determined via enzyme-linked immunosorbent assay (ELISA). A dual-luciferase reporter assay was performed to confirm the direct regulatory interactions.Results
In AD patients, the FBXL19-AS1 and integrin subunit beta 3 (ITGB3) expression were significantly elevated, whereas microRNA-650 (miR-650) expression was markedly reduced. FBXL19-AS1 showed certain diagnostic potential for AD, and its expression was negatively correlated with Montreal Cognitive Assessment (MoCA) scores. Following treatment with Aβ25-35, SH-SY5Y cells exhibited reduced proliferative capacity and increased apoptosis, while BV2 cells showed elevated levels of inflammatory factors. Additionally, Aβ25-35 treatment led to upregulated expression of FBXL19-AS1 and ITGB3, along with downregulated expression of miR-650. Knockdown of FBXL19-AS1 effectively reversed these effects. However, inhibition of miR-650 partially attenuated the changes induced by FBXL19-AS1 knockdown. Furthermore, knockdown of FBXL19-AS1 markedly reduced ITGB3 expression, whereas concurrent inhibition of miR-650 partially reversed this downregulatory effect.Conclusion
FBXL19-AS1 appears to interact with and modulate miR-650, thereby affecting ITGB3 expression and potentially participating in the pathological progression of AD.
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BibTeX
@article{dou2026lncrna,
title = {{LncRNA FBXL19-AS1 regulates the miR-650/ITGB3 axis to drive pathological progression in Alzheimer's Disease.}},
author = {Jie Dou and Yanping Zhu and Zili Du and Guangning Zhang},
journal = {Hereditas},
year = {2026},
month = aug,
doi = {10.1186/s41065-026-00727-1},
url = {https://europepmc.org/article/MED/42958467},
note = {CC BY},
}
RIS
TY - JOUR
TI - LncRNA FBXL19-AS1 regulates the miR-650/ITGB3 axis to drive pathological progression in Alzheimer's Disease.
AU - Jie Dou
AU - Yanping Zhu
AU - Zili Du
AU - Guangning Zhang
PY - 2026
DA - 2026/08/14
JO - Hereditas
DO - 10.1186/s41065-026-00727-1
UR - https://europepmc.org/article/MED/42958467
AB - Background Alzheimer's Disease (AD) is a progressive neurodegenerative disorder characterized by complex and not yet fully understood pathological mechanisms. This study was designed to explore the molecular mechanisms of long non-coding RNA (lncRNA) FBXL19-AS1 in the pathological progression of AD.Methods 110 AD patients and 110 healthy controls were recruited for this study. Relevant gene expression was measured using reverse transcription quantitative real-time PCR (RT-qPCR), and the diagnostic performance was assessed through receiver operating characteristic (ROC) curve analysis. AD cell models were established by treating SH-SY5Y and BV2 cells with amyloid β (Aβ)25-35. Cell proliferation was evaluated using the cell counting kit-8 (CCK-8) assay, cell apoptosis was analyzed by flow cytometry, and the secretion levels of inflammatory factors were determined via enzyme-linked immunosorbent assay (ELISA). A dual-luciferase reporter assay was performed to confirm the direct regulatory interactions.Results In AD patients, the FBXL19-AS1 and integrin subunit beta 3 (ITGB3) expression were significantly elevated, whereas microRNA-650 (miR-650) expression was markedly reduced. FBXL19-AS1 showed certain diagnostic potential for AD, and its expression was negatively correlated with Montreal Cognitive Assessment (MoCA) scores. Following treatment with Aβ25-35, SH-SY5Y cells exhibited reduced proliferative capacity and increased apoptosis, while BV2 cells showed elevated levels of inflammatory factors. Additionally, Aβ25-35 treatment led to upregulated expression of FBXL19-AS1 and ITGB3, along with downregulated expression of miR-650. Knockdown of FBXL19-AS1 effectively reversed these effects. However, inhibition of miR-650 partially attenuated the changes induced by FBXL19-AS1 knockdown. Furthermore, knockdown of FBXL19-AS1 markedly reduced ITGB3 expression, whereas concurrent inhibition of miR-650 partially reversed this downregulatory effect.Conclusion FBXL19-AS1 appears to interact with and modulate miR-650, thereby affecting ITGB3 expression and potentially participating in the pathological progression of AD.
SN - 0018-0661
SN - 1601-5223
ER -