Synucleins and their relationship to Parkinson’s disease

Halbach, Oliver von Bohlen und

doi:10.1007/s00441-004-0921-7

Cited by 33 publications

(28 citation statements)

References 143 publications

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“…To date, three synuclein proteins have been identified: synuclein- α (SNCA), synuclein- β (SNCB), synuclein- γ (SNCG) [5, 6]. The former two, SNCA and SNCB, have been implicated in neurodegenerative disorders, such as Parkinson’s and Alzheimer’s disease [7, 8], while SNCG has been primarily linked with cancer. SNCG was first discovered in breast cancer tissue [9] and has since been detected in multiple solid tumors, including breast, lung, liver, esophagus, colon, bladder, pancreatic, and prostate cancers [10].…”

Section: Introductionmentioning

confidence: 99%

Synuclein-γ (SNCG) expression in ovarian cancer is associated with high-risk clinicopathologic disease

et al. 2016

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BackgroundSynuclein gamma (SNCG) expression is associated with advanced disease and chemoresistance in multiple solid tumors. Our goal was to determine if SNCG protein expression in ovarian cancer was correlated with clinicopathologic variables and patient outcomes.MethodsTissue microarrays from primary tumors of 357 ovarian, fallopian tube, and primary peritoneal cancer patients, who underwent primary surgery at Roswell Park Cancer Institute between 1995 and 2007, were immunohistochemically stained for SNCG. A pathologist blinded to patient data scored tumors as positive if ≥10 % of the sample stained for SNCG. Medical records were reviewed for clinicopathologic and demographic variables. Between the positive and negative groups, Wilcoxon rank-sum test was used to compare the median ages and Fisher’s exact test was used to compare groups in categorical variables. Cox proportional hazard models examined associations between SNCG and overall and progression-free survival.ResultsThe median follow-up was 36 months, median overall survival was 39 months, and median progression-free survival was 18 months. SNCG presence was associated with clinical variables of serous histology, grade 3 disease, suboptimal debulking, ascites at surgery, FIGO stage III-IV cancer, or initial CA-125 level >485. There was no significant difference in overall survival (HR 1.06 95 % CI 0.81–1.39 P 0.69) or progression-free survival (HR 1.16 95 % CI 0.89–1.50 P 0.28) for patients with or without SNCG expression.ConclusionsSNCG expression in ovarian cancer is frequent in patients with high-risk features, but it does not correlate with chemotherapy response, overall survival, or progression-free survival.Electronic supplementary materialThe online version of this article (doi:10.1186/s13048-016-0281-4) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

Synuclein-γ (SNCG) expression in ovarian cancer is associated with high-risk clinicopathologic disease

et al. 2016

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“…SNCA and SNCB have been implicated in neurodegenerative disorders, such as Parkinson and Alzheimer disease [von Bohlen und Halbach, 2004]. In contrast, SNCG has been primarily linked with increased cancer cell proliferation, metastasis, and chemoresistance and correlated with adverse outcome in multiple solid tumors including breast, lung, liver, esophagus, colon, bladder, pancreatic, and prostate cancers Singh et al, 2008;Strohl et al, 2016].…”

Section: Introductionmentioning

confidence: 99%

siRNA Targeting of the SNCG Gene Inhibits the Growth of Gastric Carcinoma SGC7901 Cells in vitro and in vivo by Downregulating the Phosphorylation of AKT/ERK

Fan¹,

Liu²,

Tian³

et al. 2018

Cytogenet Genome Res

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The aim of the study was to evaluate the effects of synuclein-γ (SNCG) silencing on gastric cancer SGC7901 cells and to elucidate the associated mechanisms. pGCSIL-lentiviral siRNA targeting of the SNCG gene was employed to inhibit SNCG expression. Several experiments such as quantitative real-time PCR, Western blotting, MTT, colony formation, migration assay, and flow cytometry were performed to investigate the biological behavior of infected SGC7901 cells. BALB/c nude mice were used as tumor xenograft models to assess the effects of SNCG silencing on tumor growth. Western blot analysis was carried out to determine the relative levels of AKT, p-AKT, ERK, and p-ERK expression. Our results showed that SNCG was overexpressed in SGC7901 cells as compared to normal gastric mucosal epithelial cells. SGC7901 cells transfected with SNCG siRNA demonstrated significantly decreased gastric cancer growth (p < 0.01), reduced cell migration, cell cycle arrest in the G0/G1 phase, promoted tumor cell apoptosis (p < 0.01), and inhibited tumorigenesis in xenograft animal models. Western blot analysis indicated that the protein levels of p-AKT and p-ERK were much lower in the SNCG siRNA group than in the control groups. The results of the present study suggest that SNCG siRNA plays a significant role in the proliferation, migration, and tumorigenesis of gastric cancer by downregulating the phosphorylation of AKT and ERK. RNA interference-mediated silencing of SNCG may provide an opportunity to develop a novel treatment strategy for gastric cancer.

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“…The connection between mitochondria and PD has been reinforced by the finding that several of the genes that cause familial PD encode mitochondrial proteins and that mitochondrial toxins can cause PD in animals [178].…”

Section: Complex I and Parkinson's Diseasementioning

confidence: 98%

Generation of Reactive Oxygen Species by Mitochondrial Complex I: Implications in Neurodegeneration

et al. 2008

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Mitochondrial Complex I [NADH Coenzyme Q (CoQ) oxidoreductase] is the least understood of respiratory complexes. In this review we emphasize some novel findings on this enzyme that are of relevance to the pathogenesis of neurodegenerative diseases. Besides CoQ, also oxygen may be an electron acceptor from the enzyme, with generation of superoxide radical in the mitochondrial matrix. The site of superoxide generation is debated: we present evidence based on the rational use of several inhibitors that the one-electron donor to oxygen is an iron-sulphur cluster, presumably N2. On this assumption we present a novel mechanism of electron transfer to the acceptor, CoQ. Complex I is deeply involved in pathological changes, including neurodegeneration. Complex I changes are involved in common neurological diseases of the adult and old ages. Mitochondrial cytopathies due to mutations of either nuclear or mitochondrial DNA may represent a useful model of neurodegeneration. In this review we discuss Parkinson's disease, where the pathogenic involvement of Complex I is better understood; the accumulated evidence on the mode of action of Complex I inhibitors and their effect on oxygen radical generation is discussed in terms of the aetiology and pathogenesis of the disease.

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Synucleins and their relationship to Parkinson’s disease

Cited by 33 publications

References 143 publications

Synuclein-γ (SNCG) expression in ovarian cancer is associated with high-risk clinicopathologic disease

Synuclein-γ (SNCG) expression in ovarian cancer is associated with high-risk clinicopathologic disease

siRNA Targeting of the <b><i>SNCG</i></b> Gene Inhibits the Growth of Gastric Carcinoma SGC7901 Cells in vitro and in vivo<b> </b>by Downregulating the Phosphorylation of AKT/ERK

Generation of Reactive Oxygen Species by Mitochondrial Complex I: Implications in Neurodegeneration

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