ArticleCancer cell international2020
Gamma synuclein is a novel nicotine responsive protein in oral cancer malignancy.
Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- Nuclear translocation of Axl contributes to the malignancy of oral cancer cells.Journal of dental sciences · 2024Article
- MiR-34a functions as a tumor suppressor in oral cancer through the inhibition of the Axl/Akt/GSK-3β pathway.Journal of dental sciences · 2024Article
- Dissecting gastric cancer heterogeneity and exploring therapeutic strategies using bulk and single-cell transcriptomic analysis and experimental validation of tumor microenvironment and metabolic interplay.Frontiers in pharmacology · 2024Article
- A systematic review of preclinical studies evaluating the association between nicotine and the initiation and progression of cancer.Annals of translational medicine · 2023Review
- Cancer in pathologically confirmed multiple system atrophy.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2023Article
- Intragenic β-synuclein rearrangements in malignancy.Frontiers in oncology · 2023Article
- Correction to: Gamma synuclein is a novel nicotine responsive protein in oral cancer malignancy.Cancer cell international · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe mechanisms of neuronal protein γ-synuclein (SNCG) in the malignancy of oral squamous cell carcinoma (OSCC) are not clear. This study tested the hypothesis that SNCG is involved in nicotine-induced malignant behaviors of OSCC. The effect of nicotine on SNCG expression and epithelial-to-mesenchymal transition (EMT) markers were examined.
methodsShort hairpin RNA (shRNA) and an antagonist specific for α7-nicotine acetylcholine receptors (α7-nAChRs) were used to examine the role of α7-nAChRs in mediating the effects of nicotine. Knockdown of SNCG in nicotine-treated cells was performed to investigate the role of SNCG in cancer malignancy. The in vivo effect of nicotine was examined using a nude mouse xenotransplantation model.
resultsNicotine increased SNCG expression in a time- and dose-dependent manner. Nicotine treatment also increased E-cadherin and ZO-1 and decreased fibronectin and vimentin expression. After specific knockdown of α7-nAChRs and inhibition of the PI3/AKT signal, the effect of nicotine on SNCG expression was attenuated. Silencing of SNCG abolished nicotine-induced invasion and migration of OSCC cells. The xenotransplantation model revealed that nicotine augmented tumor growth and SNCG expression.
conclusionNicotine upregulated SNCG expression by activating the α7-nAChRs/PI3/AKT signaling that are participated in nicotine-induced oral cancer malignancy.
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