Abstract
Gastric cancer (GC) is one of the major malignancies worldwide. Emerging evidence has revealed the potential involvement of long noncoding RNA (lncRNA) in human genetic disorders and cancer, but the role of LOC100505817 remains unknown. Thus, in this study, we isolated tissues from GC patients to characterize the functional importance of LOC100505817 in GC tumorigenesis. We also proposed a hypothesis that the regulation of Wnt/β-catenin pathway by LOC100505817 was regulated by miR-20a-mediated WT1. After the collection of cancer tissues and adjacent tissues were obtained from GC patients, expression of LOC100505817, Wnt/β-catenin pathway- and EMT-related genes was quantified. Ectopic expression and knockdown experiments were applied in order to investigate the protective role of LOC100505817 in the progression of GC. Subsequently, cell viability, flow cytometry for apoptosis and cell cycle were detected via CCK-8, while migration and invasion were determined using scratch test and Transwell assay respectively. Then interactions among LOC100505817, miR-20a and WT1 were explored by dual luciferase reporter gene assay, RNA pull down assay and RNA binding protein immunoprecipitation (RIP) assay. The results found poor expression LOC100505817 was poorly expressed in GC cells and tissues. Overexpressed LOC100505817 resulted in the significant reduction of cell proliferation, migration and invasion as well as the expression of Wnt2b, β-catenin, CyclinD1, N-cadherin, Vimentin and snail, while increased cell apoptosis along with the expression of E-cadherin. Wnt/β-catenin pathway and EMT in GC cells were suppressed by LOC100505817 through miR-20a-inhibted WT1. In summary, our results provided evidence suggesting that LOC100505817 inhibits GC through LOC100505817-mediated inhibition of Wnt/β-catenin pathway, that leads to the overall restraining of GC cell proliferation, migration and invasion through miR-20a-reduced WT1.
Highlights
Gastric cancer (GC), one of the most prevalent cancers, remains to be the second most common cause of cancer-related mortality worldwide [1]
In order to verify the result, Reverse Transcription Quantitative Polymerase Chain Reaction (RT-qPCR) and western blot analysis were conducted for the measurement of expression patterns of Wnt2b, β-catenin, CyclinD1, N-cadherin, Vimentin, snail, LOC100505817 as well as E-cadherin in the harvested GC tumor tissues, to investigate the mechanism by which LOC100505817 and Wnt/β-catenin signaling pathway affects GC
The results of RT-qPCR are shown in Figure 1B, revealing that relative to adjacent tissues, the mRNA expression of Wnt2b, β-catenin, CyclinD1, N-cadherin, Vimentin and snail was remarkably enhanced, while LOC100505817 expression and E-cadherin mRNA expression were reduced in GC tissues
Summary
Gastric cancer (GC), one of the most prevalent cancers, remains to be the second most common cause of cancer-related mortality worldwide [1]. Several risk factors have been identified for the occurrence of GC, some of which include genetic factors, Pathology & Oncology Research. The clinical features for GC include a high risk of occurrence, unspecific clinical symptoms, increased invasive and metastatic potential, all of which contribute to the poor prognosis seen in GC patients [4]. Conventional diagnostic methods, including early diagnosis and intervention with surgical resection, have contributed to GC mortality reduction; while these methods have been found to have the highest efficacy in the management of GC, the overall survival rate remains relatively low [5, 6]. It is urgent to thoroughly explore the molecular mechanism underlying GC
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