Long non-coding RNA CERS6-AS1 plays a prognostic role in promoting the progression of gastric cancer

Figures & data

Table 1. Correlation of the lncRNA CERS6-AS1expression with clinical characteristics in GC

Indicators	Cases (n = 126)	lncRNA CERS6-AS1 expression		P
		Low (n = 60)	High (n = 66)
Age				0.598
≤ 55	64	29	35
> 55	62	31	31
Gender				0.165
Male	76	40	36
Female	50	20	30
Tumor size(cm)				0.054
<5	57	33	25
≥5	68	27	41
Local invasion				0.269
T1,T2	67	35	32
T3,T4	59	25	34
Differentiation				0.149
Well, Moderate	65	35	30
Poor	61	25	36
Lymph node metastasis				<0.001
Negative	66	49	17
Positive	60	11	49
TNM stage				<0.001
I, II	71	45	26
III, IV	55	15	40

Annotation: GC: gastric cancer.

Figure 1. The relative expression of lncRNA CERS6-AS1 in gastric cancer tissues was increased compared with normal tissues by RT-qPCR. ***P < 0.001

Figure 2. The survival probability of 60 months of low expression of lncRNA CERS6-AS1 and high expression of lncRNA CERS6-AS1 was analyzed by the Kaplan-Meier method. The survival condition of low expression of lncRNA CERS6-AS1 was significantly higher than that of a high expression of lncRNA CERS6-AS1 (log-rank P = 0.001)

Table 2. Multivariate Cox analysis of clinical characteristics in relation to overall survival

Indicators	Multivariate analysis
	HR	95% CI	P
LncRNA CERS6-AS1	4.828	2.416–9.648	<0.001
Age	1.056	0.605–1.843	0.847
Gender	1.200	0.688–2.093	0.521
Tumor size	1.545	0.901–2.651	0.114
Local invasion	1.252	0.718–2.181	0.428
Differentiation	1.269	0.729–2.208	0.399
Lymph node metastasis	2.104	1.094–4.044	0.026
TNM stage	2.053	1.119–3.768	0.020

Figure 3. Expression level of lncRNA CERS6-AS1 in different gastric cancer cell lines and analysis of transfection, proliferation, migration and invasion in gastric cancer cells HGC-27 and AGS. (a) The relative expression level of CERS6-AS1 is upregulated in different gastric cancer cells, compared with normal cells GES-1. (b) The relative expression level of CERS6-AS1 in HGC-27, and AGS cells transfected with si-CERS6-AS1 was significantly downregulated. (c) and (d) Proliferative capacity of HGC-27 and AGS cells were reduced that measured by CCK-8. (e) The Transwell assay showed that the migration ability of HGC-27, and AGS cells was down-regulated. (f) The Transwell assay showed that the invasion level of HGC-27, and AGS cells was reduced. ***P < 0.001

Figure 4. Luciferase reporter and the effect of CERS6-AS1 on miR-567. (a) The binding site of WT-CERS6-AS1 and miR-567. (b) Luciferase activity of WT-CERS6-AS1 and MUT-CERS6-AS1 in HGC-27 cells. (c) The miR-567 in gastric cancer tissues was down expressed compared with normal tissues by RT-qPCR. (d) The relative expression levels of CERS6-AS1 and miR-567 are negatively correlated. (e) The si-CERS6-AS1 obtained by knockdown CERS6-AS1 in HGC-27 cells increased the content of miR-567. ***P < 0.001

Figure 5. Co-regulated HGC-27 cells via the interaction between si-CERS6-AS1 and miR-567. HGC-27 cells were co-transfected with control, si-NC, si-CERS6-AS1, si-CERS6-AS1+ miR inhibitor NC or si-CERS6-AS1+ miR-567 inhibitor. (a) Expression of miR-567 was measured using RT-qPCR in HGC-27 cells. (b) Cell proliferation was measured by CCK-8. (c) Cell migration was analyzed using Transwell. (d) Cell invasion was analyzed using Transwell. ***P < 0.001 vs si-NC, ^###P < 0.001 vs si-CERS6-AS1+ miR inhibitor NC

Data availability statement

The corresponding author can provide relevant data for this study.