RETRACTED: MiR-142-5p Protects Against 6-OHDA-Induced SH-SY5Y Cell Injury by Downregulating BECN1 and Autophagy

Chen, Jian; Jiang, Chuan; Du, Juan; Xie, Chunli

doi:10.1177/1559325820907016

Cited by 11 publications

(5 citation statements)

References 39 publications

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“…It is reported that miR-142-5p is downregulated in 6-OHdA-treated SH-SY5Y cells, and its upregulation enhances neuronal vitality by suppressing Beclin-1-dependent autophagy, implying a neuroprotective role of miR-142-5p in the progression of Pd (72). In addition to targeting ATGs, miRNAs have been implicated in the regulation of autophagy-related signaling pathways in Pd.…”

Section: Roles Of Autophagy-regulating Mirnas In Pdmentioning

confidence: 99%

Autophagy‑regulating miRNAs: Novel therapeutic targets for Parkinson's disease (Review)

Ma¹,

Liang²,

Hu³

et al. 2023

Int J Mol Med

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Parkinson's disease (Pd) is a neurodegenerative disorder that has a high incidence during the aging process and is characterized by the loss of dopaminergic neurons in the substantia nigra, leading to motor dysfunctions and non-motor symptoms. Impaired clearance and excessive accumulation of aberrantly modified proteins or damaged organelles, such as aggregated α-synuclein and dysfunctional mitochondria, are regarded as the main causes of nigrostriatal neurodegeneration. As one of the major degradation pathways, autophagy can recycle these useless or toxic substances to maintain cellular homeostasis and it plays a crucial role in Pd progression. MicroRNAs (miRNAs) are a group of small non-coding RNA molecules that regulate gene expression by silencing targeted mRNAs. Recent studies have illustrated that autophagy-regulating miRNA has been implicated in pathological processes of Pd, including α-synuclein accumulation, mitochondrial damage, neuroinflammation and neuronal apoptosis, which suggests that targeting autophagy-regulating miRNAs may provide novel therapeutic strategies for this disease. The present review summarizes the role of autophagy in Pd and emphasizes the role of miRNA-mediated autophagy in Pd, for the development of promising interventions in this disease.

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Section: Roles Of Autophagy-regulating Mirnas In Pdmentioning

confidence: 99%

Autophagy‑regulating miRNAs: Novel therapeutic targets for Parkinson's disease (Review)

Ma¹,

Liang²,

Hu³

et al. 2023

Int J Mol Med

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“…ADAMTS9-AS1, a long-stranded non-coding RNA, inhibits the progression of PCa by regulating the miR-142-5p/CCND1 axis [30], and miRNA-186-5p inhibits the proliferation, anchorage-independent growth, and invasion of metastatic PCa cells [31]. The results highlight that miR-142-5p functions as a neuroprotective regulator in 6-OHDA-induced neuronal SH-SY5Y cells simulating the PD model in vitro via regulating autophagy-related protein beclin 1 (BECN1) and autophagy to influence cell viability [32]. Studies have shown that the downregulation of circ-CCNB2 could promote the radiosensitivity of PCa by inhibiting autophagy through the miR-30b-5p/KIF18A axis, thus establishing the molecular resistance mechanism of radiotherapy for PCa and a feasible strategy to improve radiosensitivity [33].…”

Section: Discussionmentioning

confidence: 99%

Parkinson’s Disease as a Risk Factor for Prostate Adenocarcinoma: A Molecular Point of View

Liu¹,

Yang²,

Liu³

et al. 2023

Gerontology

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Introduction: Cancer and neurodegeneration are two major leading causes of morbidity and death worldwide. Neurodegeneration results in excessive neuronal cell death, and cancer emerges from increased proliferation and resistance to cell death. Although most epidemiological studies support an inverse association between the risk for the development of neurodegenerative diseases and cancer, increasing evidence points to a positive correlation between specific types of cancer, like prostate adenocarcinoma (PRAD), and neurodegenerative diseases, like Parkinson’s disease (PD). Methods: PD and PRAD differential genes were screened through the GEO database, and the differential genes were analyzed using David, String, GEPIA, Kaplan-Meier plotter, TIMER2.0, proteinatlas, cBioPortal, and CTD databases. To elucidate the biological function and molecular mechanism of PD and PRAD-related genes. Results: Studies have shown that the hub gene and differentially expressed genes (DEGs) in PD were differentially expressed in PRAD, including CDC20, HSPA4L, ROBO1, DMKN, IFI27L2, LUZP2, PTN, PTGDS. In PRAD, the high expression of HSPA4L, ROBO1, DMKN, IFI27L2, PTN, and PTGDS genes were associated with longer survival, while the patients with low expression of CDC20 and LUZP2 genes have longer survival. The mRNA of CDC20 and LUZP2 were highly expressed, while the mRNA of HSPA4L, ROBO1, DMKN, IFI27L2, and PTGDS were low expressed. Gene methylation did not affect the survival of patients. The high expression of miR-142, miR-186, miR-30a, miR-497, miR-590, miR-28, and miR-576 in micro RNA (miRNA) might potentially be used as biomarkers for the progression of PD and PRAD, and for the early diagnosis of PD and PRAD in the populations. The genes in this study were highly associated with B cells, CD8+ T cells, CD4+ T cells, macrophages, neutrophils, and dendritic cells. Somatic mutation mainly focused on missense mutation. Therapeutic drugs included Acetaminophen and Valproic Acid (VPA). Conclusion: Bioinformatics was used to identify potential targets and novel molecular mechanisms that may serve as clinical markers for the diagnosis and treatment of PD and PRAD.

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“…SH-SY5Y cells in good conditions were treated with different concentrations (10, 50, 100, 150, and 200 μM) of 6-OHDA (Sigma-Aldrich, Merck KGaA, Darmstadt, Germany) for different time (0, 3, 6, 12, 24, and 48 h) ( Chen et al, 2020 ). The concentration and time of 6-OHDA intervention at 50% cell activity were selected as the experimental conditions.…”

Section: Methodsmentioning

confidence: 99%

Astragaloside IV Protects 6-Hydroxydopamine-Induced SH-SY5Y Cell Model of Parkinson’s Disease via Activating the JAK2/STAT3 Pathway

Xu¹,

Yang²,

Huang³

et al. 2021

Front. Neurosci.

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ObjectivesAstragaloside IV (AS-IV), the main active component of Astragalus membranaceus, bears anti-inflammatory, antioxidant, and neuroprotective activity. Parkinson’s disease (PD) is a common neurodegenerative disease. This study explored the protective effect of AS-IV on the cell model of PD.Materials and MethodsSH-SY5Y cells were incubated with different concentrations (10, 50, 100, 150, and 200 μM) of 6-hydroxydopamine (6-OHDA) for 0, 3, 6, 12, 24, and 48 h to establish the PD cell model. Different concentrations (0, 25, 50, 100, 150, and 200 μM) of AS-IV or 15 mM JAK2/STAT3 pathway inhibitor SC99 was added for intervention 2 h before 6-OHDA treatment. The viability and morphological damage of 6-OHDA-treated SH-SY5Y cells were measured using MTT assay and Hoechst 33258 staining. The expression of microtubule associated protein 2 (MAP2) was detected by immunofluorescence staining. The levels of inflammation and oxidative stress were measured using ELISA. Apoptosis of 6-OHDA-treated SH-SY5Y cells was detected using flow cytometry, and phosphorylation level of JAK2 and STAT3 were detected using Western blot analysis.ResultsThe survival rate of SH-SY5Y cells treated with 100 μM 6-OHDA for 24 h was about 50%. AS-IV (25–100 μM) significantly improved the viability (all p < 0.01), increased MAP2 expression, and repaired the morphological damage induced by 6-OHDA. AS-IV inhibited IL-1β, IL-6, and TNF-α level (all p < 0.05), reduced MDA and ROS content and increased SOD concentration, thereby reducing inflammation and oxidative stress (all p < 0.01) in 6-OHDA-treated SH-SY5Y cells. Moreover, AS-IV decreased apoptosis rate and Bax/Bcl-2 ratio induced by 6-OHDA (all p < 0.05). Mechanically, AS-IV significantly increased the phosphorylation of JAK2 and STAT3 (p < 0.01); the addition of SC99 decreased the cell viability, increased the apoptosis rate, enhanced the levels of inflammatory factors and oxidative stress.ConclusionAS-IV enhanced the cell viability, and inhibited apoptosis, inflammation and oxidative stress of 6-OHDA-treated SH-SY5Y cells via activating the JAK2/STAT3 signaling pathway. This study may confer novel insights for the management of PD.

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RETRACTED: MiR-142-5p Protects Against 6-OHDA-Induced SH-SY5Y Cell Injury by Downregulating BECN1 and Autophagy

Cited by 11 publications

References 39 publications

Autophagy‑regulating miRNAs: Novel therapeutic targets for Parkinson's disease (Review)

Autophagy‑regulating miRNAs: Novel therapeutic targets for Parkinson's disease (Review)

Parkinson’s Disease as a Risk Factor for Prostate Adenocarcinoma: A Molecular Point of View

Astragaloside IV Protects 6-Hydroxydopamine-Induced SH-SY5Y Cell Model of Parkinson’s Disease via Activating the JAK2/STAT3 Pathway

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