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. 2020 Apr 22:13:3401-3410.
doi: 10.2147/OTT.S242073. eCollection 2020.

LINC01272 Promotes Migration and Invasion of Gastric Cancer Cells via EMT

Xue Leng  1 , Geli Liu  1 , Sen Wang  2 , Jing Song  3 , Wanfeng Zhang  3 , Xianqin Zhang  1 , Li Rong  1   4 , Yongping Ma  1 , Fangzhou Song  1
Affiliations

LINC01272 Promotes Migration and Invasion of Gastric Cancer Cells via EMT

Xue Leng et al. Onco Targets Ther. .

Abstract

Purpose: Gastric cancer (GC) is the fifth most common tumor in the world, and most patients with GC have a poor prognosis. This study aimed to explore the biological influence and mechanism of LINC01272 in GC.

Materials and methods: Using bioinformatic analyses, we investigated the expression of LINC01272 in TCGA database and predicted the biological functions and mechanism of LINC01272 in GC. Then, we detected the expression of LINC01272 in GC cell lines, GC tissues, and corresponding normal tissues using real-time polymerase chain reaction (RT-PCR). Finally, we explored the migration and invasion ability of LINC01272 by wound-healing and Transwell assays and examined the expression of epithelial-mesenchymal transition (EMT)-related proteins through Western blotting.

Results: We found that LINC01272 was upregulated in GC and was associated with GC staging and lymph node metastasis. The results of wound-healing and Transwell assays revealed that the LINC01272 was closely related to GC cell migration and invasion. LINC01272 knockdown inhibited the migration and invasion ability of GC cells by reducing the expression of EMT-related proteins. Overexpression of LINC01272 had the opposite effect.

Conclusion: Together, our results showed that LINC01272 promoted GC metastasis ability by regulating the expression of EMT-related proteins and could serve as a potential diagnostic biomarker for GC.

Keywords: LINC01272; gastric cancer; invasion; long non-coding RNA; migration.

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Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Figure 1
Figure 1
Analysis of LINC01272 using bioinformatics. (A) Heat map of lncRNAs differentially expressed between GC and normal tissues. (B) Expression levels of LINC01272 in TCGA database. (C) LINC01272 expression levels in different tumor types using GEPIA online software. (D) Role of LINC01272 in GC staging. (E) Correlation analysis between LINC01272 and EMT-related factors (MMP-2, MMP-9, and TPJ1). Abbreviation: EMT, epithelial-mesenchymal transition; BLCA, bladder urothelial carcinoma; BRCA, breast invasive carcinoma; ESCA, esophageal carcinoma; KICH, kidney chromophobe; LGG, brain lower grade glioma; STAD, stomach adenocarcinoma; HNSC, head and neck squamous cell carcinoma..
Figure 2
Figure 2
LINC01272 was upregulated in GC. (A) The mRNA levels of LINC01272 were analyzed by RT-PCR in GC tissues and para-cancer tissues (***p<0.001). (B) The mRNA levels of LINC01272 were analyzed by RT-PCR in five GC cell lines (AGS, SGC7901, N87, HGC-27, and BGC823) and gastric normal epithelial cell line (GES-1). Abbreviation: RT-PCR, real-time polymerase chain reaction.
Figure 3
Figure 3
Knockdown of LINC01272 inhibited GC cell migration and invasion. (A) The expression levels of LINC01272 in BGC823 cells. BGC823 cells were transfected with siRNAs (siNC, si226, si342, and si478) and the mRNA levels of LINC01272 were detected by RT-PCR. LINC01272 was significantly downregulated in cells transfected with si342. (B) Knockdown of LINC01272 inhibited the migration of BGC823 cells, as indicated by the wound-healing assay. (C) Knockdown of LINC01272 inhibited the metastatic ability of BGC823 cells, as indicated by the Transwell migration and invasion assays. Abbreviations: siRNA, small interfering RNA; NC, normal cell.
Figure 4
Figure 4
Overexpression of LINC01272 promoted GC cell migration and invasion. (A) The expression levels of LINC01272 in AGS cells. AGS cells were transfected with overexpression plasmid and the mRNA levels of LINC01272 were verified by RT-PCR. (B) Overexpression of LINC01272 promoted the migration of AGS cells, as indicated by the wound-healing assay. (C) Overexpression of LINC01272 promoted the metastatic ability of AGS cells, as indicated by the Transwell migration and invasion assays. Abbreviations: RT-PCR, real-time polymerase chain reaction; NC, normal cell.
Figure 5
Figure 5
The expression of EMT-related transcription factors. (A) Knockdown of LINC01272 inhibited the expression of EMT-related proteins (MMP-9, N-CAD, ZEB2, and vimentin). (B) Upregulation of LINC01272 enhanced the expression of EMT-related proteins (MMP-9, N-CAD, Twist, and ZEB2). Abbreviations: NC, normal cell; MMP-9, matrix metallopeptidase 9; N-CAD, cadherin 2; ZEB2, zinc finger E-box binding homeobox 2.
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