Overexpression of long non‐coding RNA RP11‐363E7.4 inhibits proliferation and invasion in gastric cancer

Abstract

LncRNA RP11-363E7.4 has been shown to be downregulated in gastric cancer (GC), while the effect of lncRNA RP11-363E7.4 on GC and its potential molecular mechanisms is unclear. The purpose of this study was to explore the functional role and underlying molecular mechanisms of lncRNA RP11-363E7.4 involved in GC progress. To address the question, quantitative real-time PCR assay was performed to confirm lncRNA RP11-363E7.4 expression levels in GC tissues and cell lines. Cell proliferation, apoptosis, migration and invasion were estimated using Cell Counting Kit-8, colony formation, scratch wound healing and Transwell assays. Potential molecular mechanisms were evaluated using western blot assay. The results showed that lncRNA RP11-363E7.4 was significantly downregulated in GC cell lines and 82 paired tissues. The correlation between expression and clinicopathological features indicated that low expression of lncRNA RP11-363E7.4 was associated with T stage (P = .010). Functional experiments showed that overexpression of lncRNA RP11-363E7.4 prevented proliferation, migration, and invasion and induced apoptosis of GC cells. Western blot assay revealed that lncRNA RP11-363E7.4 functioned via the p53, Bax/Bcl-2, β-catenin pathway. In summary, this study revealed that lncRNA RP11-363E7.4 functioned as a tumour suppressor by inhibiting proliferation, migration, and invasion and inducing apoptosis of GC cells. Significance of the study: LncRNA RP11-363E7.4 has been shown to be downregulated in GC, while the effect of lncRNA RP11-363E7.4 on GC and its potential molecular mechanism is unclear. We revealed that lncRNA RP11-363E7.4 functioned as a tumour suppressor by inhibiting proliferation, migration, and invasion and inducing apoptosis of GC cells. LncRNA RP11-363E7.4 might become an attractive diagnostic and prognostic biomarker of GC and a promising target for GC treatment.

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“…12,13 For example, lncRNA RP11-363E7.4 inhibits gastric cancer cell proliferation and invasion. 14 LncRNA HAND2-AS1 suppresses liver cancer progression through inactivating the JAK-STAT signaling. 15 Importantly, the biological role and regulatory function of lncRNAs in CRC are also identified.…”

DoxoDB: A Database for the Expression Analysis of Doxorubicin-Induced lncRNA Genes

“…It has been reported to be involved in fibrogenesis in idiopathic pulmonary fibrosis [ 79 ] and found to be dysregulated in patients with myocardial infarction and atrial fibrillation [ 80 , 81 ]. Furthermore, studies have reported its dysregulation in two colon carcinoma cell lines (SW480 and Caco2) upon knockdown of the aurora kinase A ( AURKA ) gene [ 82 ], in papillary thyroid carcinoma [ 83 ], in hepatocellular carcinoma treated with cisplatin [ 84 ], and in gastric cancer [ 85 , 86 ]. Another novel transcript ENSG00000272468 (also known as Lnc-HIST1H2BJ-3 ) [ 87 ] and MAP3K4-AS1 [ 88 ] were reported to be dysregulated in stomach adenocarcinoma and in breast cancer, respectively.…”

Repurposing Niclosamide as a Therapeutic Drug against Acute Liver Failure by Suppressing Ferroptosis

“…Hub nodes of ferroptosis-related regulatory networks comprising four lncRNAs, five miRNAs, and one mRNA were identified, indicating their importance in regulating ferroptosis and implying their role as potential biomarkers or drug targets in patients with ALF. Among these ten hub nodes identified, RP11-363E7.4, miR-106a-5p, miR-3666, miR-665, miR-590-5p, and STMN1 facilitate cell death, whereas miR-4295 inhibits apoptosis in human glioma cell lines [ 58 , 59 , 60 , 61 , 62 , 63 , 64 ]. miRNA-106a-5p, which is directly targeted by four other lncRNAs in the hub nodes, was sponged and downregulated in breast cancer cells, leading to inhibition of ferroptosis [ 65 ].…”