[shRNA-Mediated Suppression of γ-Synuclein Leading to Downregulation of p38/ERK/JNK Phosphorylation and Cell Cycle Arrest in Endometrial Cancer Cells].

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  • Additional Information
    • Source:
      Publisher: Izdatelstvo Nauka Country of Publication: Russia (Federation) NLM ID: 0105454 Publication Model: Print Cited Medium: Print ISSN: 0026-8984 (Print) Linking ISSN: 00268984 NLM ISO Abbreviation: Mol Biol (Mosk) Subsets: MEDLINE
    • Publication Information:
      Original Publication: Moskva : Izdatelstvo Nauka
    • Subject Terms:
      Cell Cycle Checkpoints* ; Endometrial Neoplasms*/genetics ; Endometrial Neoplasms*/pathology ; Extracellular Signal-Regulated MAP Kinases*/metabolism; Neoplasm Proteins/*genetics ; RNA, Small Interfering/*genetics ; gamma-Synuclein/*genetics; Cell Line, Tumor ; Cell Proliferation/genetics ; Down-Regulation ; Female ; Humans ; Phosphorylation ; p38 Mitogen-Activated Protein Kinases/genetics ; p38 Mitogen-Activated Protein Kinases/metabolism
    • Abstract:
      In this study, we explored the effects of treating human endometrial cancer cells with γ-synuclein-specific short hairpin RNA (shRNA) and elucidated the associated mechanisms in vitro and in vivo through the p38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK) signaling pathways. Cell proliferation and migration were assessed using CCK8, Transwell, and scratch wound healing assays. Flow cytometry and laser scanning confocal microscopy were used to detect cell cycle changes. Relative levels of phosphorylated and non-phosphorylated (p) p38, ERK1/2 and JNK1/2/3 were determined in vitro and in vivo using simple western blotting assays. Cell proliferation in the experimental group decreased significantly and cells transfected with shRNA showed reduced migration rates (P < 0.05). p-p38, p-ERK1/2, and p-JNK1/2/3 levels were downregulated in the experimental group in vitro and in vivo. Tumor volumes and weights in the experimental group were significantly lower (P < 0.05). Tumor formation time in the negative control group was significantly shorter (P < 0.05). Flow cytometry showed that the number of cells in the G1 and mitotic phases increased and that in the S phase decreased after SNCG silencing (P < 0.05). Confocal microscopy showed that the percentage of cells in the mitotic phase increased after SNCG gene silencing (P < 0.05). We conclude that shRNA-mediated suppression of γ-synuclein decreased the proliferation, migration, and tumorigenicity of endometrial cancer cells via downregulation of p38, ERK, and JNK phosphorylation. High SNCG expression is closely related to the growth cycle of endometrial cancer cells.
    • Contributed Indexing:
      Keywords: ERK; JNK; SNCG; endometrial cancer; p38; γ-synuclein
    • Accession Number:
      0 (Neoplasm Proteins)
      0 (RNA, Small Interfering)
      0 (SNCG protein, human)
      0 (gamma-Synuclein)
      EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
      EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
    • Publication Date:
      Date Created: 20201204 Date Completed: 20201209 Latest Revision: 20201214
    • Publication Date:
      20240829
    • Accession Number:
      10.31857/S0026898420060117
    • Accession Number:
      33276364