Abstract
BackgroundThe aim of this study was to investigate the role of long non-coding RNA (lncRNA) H19 in gastric cancer (GC) with Helicobacter pylori (H. pylori).MethodsH19 expression in peripheral blood from H. pylori+/− GC patients and healthy donors (control) as well as in GC tissues and cells were detected by qRT-PCR. Cell proliferation was evaluated by CCK-8 assay. Cell migration and invasion were evaluated by Transwell assay. The levels of pro-inflammatory cytokines were determined by ELISA. The protein levels of IκBα, p-IκBα and p65 were determined by western blotting.ResultsH19 expression was upregulated in H. pylori-infected GC tissues and cells. Furthermore, H. pylori promoted GC cell viability, migration, invasion and inflammatory response. Moreover, H19 overexpression promoted the proliferation, migration and invasion of H. pylori-infected GC cells via enhancing NF-κB-induced inflammation.ConclusionsLncRNA H19 promotes H. pylori-induced GC cell growth via enhancing NF-κB-induced inflammation.
Highlights
The aim of this study was to investigate the role of long non-coding RNA H19 in gastric cancer (GC) with Helicobacter pylori (H. pylori)
H19 was upregulated in HP-infected GC tissues and cells Quantitative real-time PCR (qRT-PCR) analysis showed that serum H19 expression was significantly higher in HP +/− GC patients relative to control donors, and higher H19 expression was observed in HP+ group compared with HP- group (Fig. 1a)
H19 expression was significantly upregulated in GC tumors from both in HP+ and HP- patients relative to adjacent tissues, and H19 expression was prominently upregulated in HP+ tissues compared with HP- group (Fig. 1b)
Summary
The aim of this study was to investigate the role of long non-coding RNA (lncRNA) H19 in gastric cancer (GC) with Helicobacter pylori (H. pylori). Results: H19 expression was upregulated in H. pylori-infected GC tissues and cells. H. pylori promoted GC cell viability, migration, invasion and inflammatory response. H19 overexpression promoted the proliferation, migration and invasion of H. pylori-infected GC cells via enhancing NF-κB-induced inflammation. Conclusions: LncRNA H19 promotes H. pylori-induced GC cell growth via enhancing NF-κB-induced inflammation. HP is considered to be the most common etiologic agent for infection-related cancers, Zhang et al Journal of Inflammation (2019) 16:23 or an encoded protein [16, 17]. Our previous work showed that H19 was increased in GC cell lines and tissues, and H19 overexpression promoted gastric cell proliferation and inhibited cell apoptosis, whereas H19 knockdown yielded the opposite results [19]. We investigated the role of H19 in regulating proliferation, migration and invasion of HP-induced GC cells. We elucidated whether the underlying mechanism was associated with its regulation of NF-κB signaling pathway
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