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Updated: Aug 14, 2026

RNA Pull-down Procedure to Identify RNA Targets of a Long Non-coding RNA
Published on: April 10, 2018
Identification of the biological affection of long noncoding RNA BC200 in Alzheimer's disease
Abstract:
BC200 is a long noncoding RNA expressed at high levels in the Alzheimer's disease (AD), and blocking of BC200 by siRNA is assumed to be an effective method for various disease therapy. We have established an AD cell model overexpressing amyloid β-peptide (Aβ)1-42 to observe the effects of BC200 on the cell viability and apoptosis, and to investigate the associated underlying mechanisms. Efficient knockdown and overexpression of BC200 were established using BC200 siRNA and BC200 mimics, respectively. Cell viability following BC200 knockdown and overexpression was assessed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyltetrazolium bromide assay, and cell apoptosis was monitored by flow cytometry. We successfully established an AD cell model overexpressing Aβ1-42 gene, and reported the results of change of BC200 on Aβ1-42 levels. Knockdown of BC200 significantly suppressed b-site amyloid precursor protein-cleaving enzyme 1 (BACE1) expression, and overexpression of BC200 increased BACE1 expression. Besides, inhibition of BC200 significantly increased cell viability and reduced cell apoptosis in the AD model via directly targeting BACE1, which can be increased by overexpression of BC200. BC200 regulated AD cell viability and apoptosis via targeting BACE1, and it may be one of the putative target in AD development and provides potential new insights into genetic therapy against AD.
Insights
Blocking the long noncoding RNA BC200 with siRNA shows promise for Alzheimer's disease (AD) therapy. Inhibiting BC200 enhances cell viability and reduces apoptosis in AD models by targeting BACE1.
Area of Science:
- Molecular Biology
- Neuroscience
- Genetics
Background:
- Alzheimer's disease (AD) is a neurodegenerative disorder characterized by amyloid-beta (Aβ) peptide accumulation.
- Long noncoding RNAs (lncRNAs) are increasingly implicated in disease pathogenesis, with BC200 found at high levels in AD.
- Therapeutic strategies targeting lncRNAs like BC200 are under investigation for AD treatment.
Purpose of the Study:
- To investigate the role of BC200 in an Alzheimer's disease cell model.
- To determine the effect of BC200 modulation on cell viability and apoptosis.
- To elucidate the underlying molecular mechanisms, particularly the involvement of BACE1.
Main Methods:
- Establishment of an AD cell model overexpressing amyloid-beta (Aβ)1-42.
- Modulation of BC200 levels using siRNA (knockdown) and mimics (overexpression).
- Assessment of cell viability via MTT assay and apoptosis via flow cytometry.
- Measurement of BACE1 expression levels.
Main Results:
- BC200 knockdown significantly suppressed BACE1 expression in the AD model.
- BC200 overexpression led to increased BACE1 expression.
- Inhibition of BC200 enhanced cell viability and reduced apoptosis in the AD model.
- BC200 directly targets and regulates BACE1, influencing AD pathology.
Conclusions:
- BC200 plays a significant role in regulating cell viability and apoptosis in Alzheimer's disease.
- Targeting BC200, potentially via BACE1, offers a novel therapeutic strategy for AD.
- BC200 represents a potential therapeutic target for genetic interventions in Alzheimer's disease.
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