Abstract
The long non-coding RNA (lncRNA) SNHG3 has been shown to play oncogenic roles in several cancer types, but the mechanisms underlying its activity are poorly understood. In this study, we aimed to explore the clinical relevance and mechanistic role of SNHG3 in gastric cancer (GC). We found that SNHG3 expression in GC cell lines and tissues was significantly increased, and the upregulation of this lncRNA was correlated with tumor clinical stage and decreased patient survival. Knocking down SNHG3 in GC cells impaired the proliferative, migratory, and invasive activity in vitro and constrained in vivo GC xenograft tumor growth. Mechanistically, SNHG3 was found to bind and sequester miR-139-5p, thereby indirectly promoting the upregulation of the miR-139-5p target gene MYB. These data demonstrated that SNHG3 functions in an oncogenic manner to drive GC proliferation, migration, and invasion by regulating the miR-139-5p/MYB axis.
Highlights
Gastric cancer (GC) is the third most prevalent form of cancer globally [1,2,3]
Research suggests that long non-coding RNA (lncRNA) can bind to these miRNAs via sequence complementarity, serving as competing endogenous RNAs that thereby disrupt the ability of given miRNA to suppress the expression of its target mRNA [9,10,11]
Www.aging-us.com www.aging-us.com www.aging-us.com www.aging-us.com www.aging-us.com www.aging-us.com dysregulation has been closely linked to oncogenesis and cancer progression, the mechanisms governing many of these regulatory relationships remain to be defined
Summary
The majority of GC patients are diagnosed with advanced disease as it causes few symptoms in its early stages [1]. Recent advances in sequencing technologies have indicated that the majority of the human genome is made up of non-coding RNAs (ncRNAs), with long ncRNAs (lncRNAs) being those > 200 nucleotides in length [6]. These lncRNAs can regulate diverse cellular processes under physiological and pathological conditions, contributing to oncogenesis and tumor malignancy [7]. Research suggests that lncRNAs can bind to these miRNAs via sequence complementarity, serving as competing endogenous RNAs (ceRNAs) that thereby disrupt the ability of given miRNA to suppress the expression of its target mRNA [9,10,11]
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