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Research Paper

LncRNA LINC01270 aggravates the progression of gastric cancer through modulation of miR-326/EFNA3 axis

, , , &
Pages 8995-9006 | Received 17 Nov 2021, Accepted 11 Mar 2022, Published online: 29 Mar 2022

Figures & data

Figure 1. LINC01270 expression was up-regulated in GC.

(a) The expression of LINC01270 was examined in GC tissues and normal adjacent tissues through RT-qPCR. (b) The expression of LINC01270 was measured in gastric epithelial cell (GES-1) and GC cell lines (HGC-27, AGS, and SGC-7901) through RT-qPCR. (c) The location of LINC01270 in tumor tissues or normal tissues was verified through RNA-FISH. ***p < 0.001.
Figure 1. LINC01270 expression was up-regulated in GC.

Figure 2. LINC01270 knockdown retarded GC progression.

(a) The knockdown efficiency of LINC01270 was verified in the sh-NC, sh-LINC01270#1, sh-LINC01270#2, and sh-LINC01270#3 groups through RT-qPCR. (b) The cell viability was detected after silencing LINC01270 through CCK-8 assay. (c) The cell proliferation was measured after silencing LINC01270 through colony formation assay. (d and e) The cell migration and invasion abilities were assessed after silencing LINC01270 through Transwell assay. ***p < 0.001.
Figure 2. LINC01270 knockdown retarded GC progression.

Figure 3. LINC01270 suppression reduced tumor growth in vivo.

(a–c) The tumor size, volume, and weight in nude mice were detected. (d) The Ki-67 expression was examined through IHC assay. ***p < 0.001.
Figure 3. LINC01270 suppression reduced tumor growth in vivo.

Figure 4. LINC01270 sponged miR-326.

(a) The binding sites between LINC01270 and miR-326. (b and c) The binding ability between LINC01270 and miR-326 was confirmed through luciferase reporter and RAN pull-down assays. (d) The expression of miR-326 was tested after silencing LINC01270 through RT-qPCR. (e) The expression of miR-326 was examined in GC tissues and normal adjacent tissues through RT-qPCR. (f) The correlation between LINC01270 and miR-326 was verified. ***p < 0.001.
Figure 4. LINC01270 sponged miR-326.

Figure 5. MiR-326 targeted and regulated EFNA3.

(a) The binding sites between miR-326 and EFNA3. (b and c) The binding ability between miR-326 and EFNA3 was confirmed through luciferase reporter and RAN pull-down assays. (d and e) The EFNA3 mRNA and protein expressions were detected after overexpressing miR-326 through RT-qPCR and western blot. (f) The expression of EFNA3 was evaluated in GC tissues and normal adjacent tissues through RT-qPCR. (g) The correlation between miR-326 and EFNA3 was confirmed. (h and i) The mRNA and protein expressions of EFNA3 were examined in the control, sh-LINC01270, sh-LINC01270+miR-inhibitor NC, and sh-LINC01270+miR-326 inhibitor through RT-qPCR and western blot. ***p < 0.001; ###p < 0.001 vs sh-LINC01270+miR-inhibitor NC.
Figure 5. MiR-326 targeted and regulated EFNA3.

Figure 6. LINC01270 affected GC progression via miR-326/EFNA3 axis.

Groups were divided into the control, sh-LINC01270, sh-LINC01270+miR-inhibitor NC, sh-LINC01270+miR-326 inhibitor, sh-LINC01270+pcDNA-NC, and sh-LINC01270+EFNA3 groups. (a and b) The mRNA and protein expressions of EFNA3 were evaluated through RT-qPCR and western blot. (c and d) The cell proliferation was detected through CCK-8 and colony formation assays. (e and f) The cell migration and invasion abilities were examined through Transwell assay. ***p < 0.001 vs sh-NC.###p < 0.001 vs sh-LINC01270+miR-inhibitor NC; &&&p < 0.001 vs sh-LINC01270+pcDNA-NC.
Figure 6. LINC01270 affected GC progression via miR-326/EFNA3 axis.
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Data availability statement

The authors confirm that the data supporting the findings of this study are available within the article.