Long non-coding RNA PCED1B antisense RNA 1 promotes gastric cancer progression via modulating microRNA-215-3p / C-X-C motif chemokine receptor 1 axis

Abstract

Long non-coding RNAs (lncRNAs) emerge as vital modulators and tissue-specific biomarkers of multiple cancers, including gastric cancer (GC). Instead, the expression characteristics, biological function and molecular mechanism of lncRNA PCED1B antisense RNA 1 (PCED1B-AS1) in GC await more elaboration. In this study, 48 cases of GC tissues and matched non-cancerous tissues were collected, and PCED1B-AS1, microRNA-215-3p (miR-215-3p) and C-X-C motif chemokine receptor 1 (CXCR1) expression levels were detected by qRT-PCR. Besides, CCK-8, EdU, Transwell and Western blot assays were conducted to assess the impact of PCED1B-AS1 or miR-215-3p on cell growth, migration, invasion and epithelial-mesenchymal transition (EMT). The interaction between genes was verified by bioinformatics analysis, rna immunoprecitipation (RIP) and dual-luciferase reporter gene assays. We demonstrated that, PCED1B-AS1 expression level was raised in GC tissues and cell lines, and increased expression of PCED1B-AS1 was in association with tumor size, TNM stage and lymph node metastasis in GC patients. Additionally, PCED1B-AS1 overexpression promoted GC cells proliferation, migration, invasion and EMT, and miR-215-3p overexpression counteracted the biological effects of PCED1B-AS1. Mechanistically, PCED1B-AS1 specifically inhibited miR-215-3p expressions, thus up-regulating CXCR1 expressions. In conclusion, PCED1B-AS1 accelerates GC progression via adsorbing miR-215-3p and up-regulating CXCR1, indicating that PCED1B-AS1 is a novel therapeutic target for treating GC.

Upregulation of PCED1B-AS1 in proliferative diabetic retinopathy and its involvement in retinal vascular endothelial cell proliferation

“…Additionally, this study observed that PCED1B-AS1 significantly attenuated the upregulation of MCP-1 induced by the CoCl 2 or TNF-α in Müller cells. Our findings are in agreement with previous studies which demonstrated that PCED1B-AS1 modulates chemokine receptors and immunosuppression [ 38 , 39 ]. The fact that PCED1B-AS1 had no effect on the upregulation of MCP-1 induced by the 25mM glucose may indicate that PCED1B-AS1 has a particular influence on the oxidative stress induced by continuous high glucose, instead of high glucose itself.…”

LncRNA PCED1B-AS1 mediates miR-3681-3p/MAP2K7 axis to promote metastasis, invasion and EMT in gastric cancer

“…LncRNA NORAD promotes gastric cancer cell proliferation by regulating miR-608 and affecting FOXO6 protein expression [ 19 ]. Ren et al [ 20 ] reported that PCED1B-AS1 accelerated GC progression via adsorbing miR-215-3p and up-regulating CXCR1, indicating that PCED1B-AS1 is a novel therapeutic target for treating GC. Likewise, we further studied the downstream miRNAs of lncRNA PCED1B-AS1 and found specific binding sites between PCED1B-AS1 and miR-3681-3p.…”

Kinesin family member 2A links with advanced tumor stage, reduced chemosensitivity and worse prognosis in gastric cancer

“…At 24 h after completion of transfection, all cells (KD‐KIF2A, KD‐NC, blank) were treated with capecitabine (Sigma‐Aldrich) and oxaliplatin (Sigma‐Aldrich), respectively. The concentrations of chemotherapeutic agents were set partly according to a previous study 19 with some modification as follows: capecitabine, 0, 100, 200, 400, 800, 1600, and 3200 μg/ml; oxaliplatin, 0, 0.2, 0.4, 0.8, 1.6, 3.2, and 6.4 μM. For the determination of drug sensitivity of cells, the relative cell viability at each drug concentration was measured after treatment for 48 h, with the use of Cell Counting Kit‐8 (Beyotime) according to the instruction of the kit.…”