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http://purl.uniprot.org/citations/30556865http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
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Objective

The aim of this study was to investigate the function of FAL1 in gastric cancer (GC) development and to examine its underlying mechanism. Our study might provide a theoretical basis for developing novel diagnostic markers for GC.

Patients and methods

FAL1 expression in GC tissues and adjacent tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The serum level of FAL1 in GC patients with different pathological grades was further detected. The effects of FAL1 on cell proliferation and cell cycle were detected by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. Meanwhile, Western blot was used to detect the protein expression of PTEN after FAL1 overexpression or knockdown in GC cells. In addition, rescue experiments were conducted to verify the regulatory effect of FAL1 on PTEN.

Results

QRT-PCR results showed that the expression of FAL1 in GC tissues was remarkably higher than that of adjacent tissues. FAL1 expression was correlated with pathological grades of GC patients. Meanwhile, FAL1 overexpression promoted the proliferation and cell cycle of BGC-823 and MGC-803 cells. Western blot analysis demonstrated that FAL1 could inhibit the protein expression of PTEN in GC cells. In addition, rescue experiments indicated that the overexpression of PTEN could partially reverse the effect of FAL1 on the proliferation and cell cycle of BGC-823 and MGC-803 cells.

Conclusions

The overexpression of FAL1 can promote cell proliferation and cell cycle of GC via inhibiting PTEN."xsd:string
http://purl.uniprot.org/citations/30556865http://purl.org/dc/terms/identifier"doi:10.26355/eurrev_201812_16520"xsd:string
http://purl.uniprot.org/citations/30556865http://purl.uniprot.org/core/author"Zhu C.H."xsd:string
http://purl.uniprot.org/citations/30556865http://purl.uniprot.org/core/author"Jiang Y.H."xsd:string
http://purl.uniprot.org/citations/30556865http://purl.uniprot.org/core/author"Zheng Z.J."xsd:string
http://purl.uniprot.org/citations/30556865http://purl.uniprot.org/core/author"Xu H.G."xsd:string
http://purl.uniprot.org/citations/30556865http://purl.uniprot.org/core/author"Dai L.G."xsd:string
http://purl.uniprot.org/citations/30556865http://purl.uniprot.org/core/author"Xiao D.H."xsd:string
http://purl.uniprot.org/citations/30556865http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/30556865http://purl.uniprot.org/core/name"Eur Rev Med Pharmacol Sci"xsd:string
http://purl.uniprot.org/citations/30556865http://purl.uniprot.org/core/pages"8257-8264"xsd:string
http://purl.uniprot.org/citations/30556865http://purl.uniprot.org/core/title"Highly expressed lncRNA FAL1 promotes the progression of gastric cancer by inhibiting PTEN."xsd:string
http://purl.uniprot.org/citations/30556865http://purl.uniprot.org/core/volume"22"xsd:string
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