Background: Long non-coding RNAs have been acknowledged as the crucial regulators in the progression of human cancers, including gastric cancer (GC). Small nucleolar RNA host gene 10 (SNHG10) has been identified as an oncogene in several cancer types. Nonetheless, it is unclear whether SNHG10 exerts functions in GC cells.
Aims: The aims of the current study were to explore the function and underlying mechanism of SNHG10 in GC.
Methods: The expression levels of SNHG10, miR-495-3p and catenin beta 1 (CTNNB1) were detected by RT-qPCR. Loss-of-function assays, including CCK-8, colony formation assay, flow cytometry analysis and transwell assays, were conducted to verify the effect of SHNG10 on the proliferation, apoptosis, migration and invasion of GC cells. Mechanism experiments were performed to identify the downstream molecular mechanism of SNHG10.
Results: SNHG10 was expressed at a high level in GC cells. Knockdown of SNHG10 inhibited the proliferation, migration and invasion of GC cells. Silencing of SNHG10 led to the downregulation of core factors of WNT signaling pathway. Knockdown of SNHG10 could decline the expression of CTNNB1 through sequestering miR-495-3p.
Conclusions: SNHG10 promotes the procession of GC through targeting miR-495-3p/CTNNB1 and activating WNT signaling pathway.
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http://dx.doi.org/10.1007/s10620-020-06576-w | DOI Listing |
Cell Signal
January 2025
Department of Obstetrics and Gynecology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330008, Jiangxi, China. Electronic address:
Small nucleolar RNA host gene 10 (SNHG10) is a newly recognized long non-coding RNA (lncRNA) with significant implications in cancer biology. Abnormal expression of SNHG10 has been observed in various solid tumors and hematological malignancies. Research conducted in vivo and in vitro has revealed that SNHG10 plays a pivotal role in numerous biological processes, including cell proliferation, apoptosis, invasion and migration, drug resistance, energy metabolism, immune evasion, as well as tumor growth and metastasis.
View Article and Find Full Text PDFPeerJ
December 2024
Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases of Ministry of Education, Gannan Medical University, Ganzhou, China.
Ischemic stroke (IS) remains a leading cause of disability and mortality worldwide, and inflammation and oxidative stress play significant roles in its pathogenesis. This study investigates the effects of dihydromyricetin (DHM) on IS using RT-qPCR and western blot with SH-SY5Y cells, focusing on its effects on the small nucleolar RNA host gene 10 (SNHG10)/microRNA (miR)-665/Ras association domain family member 5 (RASSF5) axis and nuclear factor-kappa B (NF-κB) signaling. In addition, the effects of the SNHG10/miR-665/RASSF5 axis on SH-SY5Y cell activity, apoptosis, oxidative stress, and inflammatory markers were analyzed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry, and enzyme-linked immunosorbent assays.
View Article and Find Full Text PDFJ Integr Neurosci
October 2023
Department of Basic Medicine, Hebei North University, 075000 Zhangjiakou, Hebei, China.
Background: Alzheimer's disease (AD) occurs in the elderly and pre-elderly, characterized by decline of memory, cognitive dysfunction, impairment of learning capacity, and motor dysfunction. Recently a competitive endogenous RNA (ceRNA) network has been found to be related to AD progression, but there is still little understanding of the ceRNA regulatory network in AD. This study aims to explore the important regulatory mechanisms of ceRNA regulatory networks containing long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), microRNAs (miRNAs), and messenger RNAs (mRNAs) in AD.
View Article and Find Full Text PDFToxicol In Vitro
February 2024
Department of Anesthesiology, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan 030032, Shanxi, China; Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, China.
Myocardial infarction (MI) has been considered a leading cause of death worldwide. Relieving ischemia-reperfusion myocardial damage is one of the major roles in treating MI. Sevoflurane postconditioning provides myocardial protection, and this study probes the mechanism of sevoflurane-mediated protective effects.
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