Long non‑coding RNA NEAT1 increases the aggressiveness of gastric cancer by regulating the microRNA‑142‑5p/JAG1 axis
- Yanming Zhang
- Liying Chang
- Qunmei Wu
- Fang Zuo
Affiliations: Department of General Medicine, Yantaishan Hospital, Yantai, Shandong 264001, P.R. China, Health Management Center, Qingdao Tumor Hospital, Qingdao, Shandong 266042, P.R. China, Health Management Center, Qingdao Central Hospital, Qingdao, Shandong 266042, P.R. China, Department of Gastroenterology, Jinan Central Hospital, Jinan, Shandong 250010, P.R. China
- Published online on: June 10, 2021 https://doi.org/10.3892/etm.2021.10294
Copyright: © Zhang
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Gastric cancer has been indicated to have a high recurrence rate in China. Previous studies have revealed that long non‑coding RNA nuclear‑enriched abundant transcript 1 (NEAT1) exerted critical roles in cancers. Therefore, the present study aimed to determine the function of NEAT1 and explore the unknown molecular mechanisms of gastric cancer pathogenesis. Reverse transcription‑quantitative PCR assay was used to examine the expression of NEAT1, microRNA (miR)‑142‑5p and jagged1 (JAG1) in gastric cancer. Cell Counting Kit‑8 and Transwell assays were conducted to examine cell proliferation, migration and invasion. The protein expression levels of N‑cadherin, Vimentin, E‑cadherin and JAG1 were quantified by western blot assay. The associations among NEAT1, miR‑142‑5p and JAG1 were confirmed by dual‑luciferase reporter assay and RNA immunoprecipitation. The effects of NEAT1 silencing on tumor growth were evaluated by tumor xenografts. The results indicated that NEAT1 was highly expressed in tumor tissues and cells compared with that in paracancerous tissues and the normal gastric epithelial cell line GES‑1 and significantly associated with poor prognosis in gastric cancer. Functional analyses further demonstrated that NEAT1 knockdown suppressed proliferation, motility and tumor growth in vitro and in vivo. Mechanistically, NEAT1 sponged miR‑142‑5p to regulate JAG1 expression. In addition, the effects of NEAT1 knockdown on the proliferation, migration and invasion of gastric cancer cells could be rescued by miR‑142‑5p inhibitor, and JAG1 overexpression reversed the miR‑142‑5p‑mediated effects on gastric cancer cells. These findings demonstrated that long non‑coding RNA NEAT1 regulated gastric cancer progression by targeting the miR‑142‑5p/JAG1 axis.