Abstract
The long intergenic non-coding RNA linc01133 is reported to be oncogenic in various malignancies. However, the role and mechanism of linc01133 in regulating gastric cancer growth is still not clear. In the present study, we found that linc01133 was significantly upregulated in gastric cancer tissues compared to non-tumorous gastric tissues. Linc01133 over-expression significantly correlated with tumor size and tumor differentiation in gastric cancer patients. The expression of linc01133 was regulated by c-Jun and c-Fos collaboratively. In both in vitro and in vivo studies, linc01133 was shown to promote gastric cancer cell growth. Linc01133 localized in the cytoplasm and functioned as an endogenous competing RNA of miR-145-5p to upregulate the expression of YES1, which was proved to be the target gene of miR-145-5p. By promoting YES1-dependent YAP1 nuclear translocation, linc01133 upregulated the expression of the key cell cycle regulators CDK4, CDK6 and cyclin D1 to promote G1-S phase transition. Thus, our study unveiled the function and mechanism of linc01133 regulating cell cycle progression in gastric cancer.
Highlights
Gastric cancer (GC) is one of the leading causes of malignancyassociated deaths
Linc01133 is upregulated in gastric cancer tissues Previously, Long noncoding RNAs (lncRNAs) microarray was performed on 10 gastric cancer tissues and 2 normal gastric tissues by our team (GSE72307)
We subsequently confirmed the upregulation of linc01133 by 2.54-fold in gastric cancer tissues compared to
Summary
Gastric cancer (GC) is one of the leading causes of malignancyassociated deaths. much has been improved in disease diagnosis and treatment, the prognosis of patients with GC in advanced stages remains non-optimistic. Increasing numbers of studies have indicated that lncRNAs play key roles in tumorigenesis and may be used in the diagnosis of cancers [3]. It was reported that linc01133 plays oncogenic roles in pancreatic cancer, hepatocellular carcinoma, renal cell carcinoma, endometrial carcinoma and cervical squamous carcinoma, while in colorectal carcinoma, linc01133 inhibits the malignant progression [5, 6]. It is not well understood how linc01133 regulate the growth of gastric cancer cells. We found that linc01133 was significantly upregulated in gastric cancer tissues compared to non-tumorous gastric tissues. Linc01133 upregulated the expression of the key cell cycle regulators such as CDK4, CDK6 and cyclin D1 by enhancing YES1-dependent YAP1 nuclear translocation to promote cell cycle progression
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