4.5 Article

lncRNA ELFN1-AS1 upregulates TRIM29 by suppressing miR-211-3p to promote gastric cancer progression

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ACTA BIOCHIMICA ET BIOPHYSICA SINICA
卷 55, 期 3, 页码 484-497

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SCIENCE PRESS
DOI: 10.3724/abbs.2023023

关键词

ELFN1-AS1; TRIM29; migration; invasion; proliferation; interplay

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The study found that long noncoding RNA (lncRNA) extracellular leucine rich repeat and fibronectin type III domain containing 1-antisense RNA 1 (ELFN1-AS1) is upregulated in various tumors. However, its role in gastric cancer (GC) is not well understood. The study showed that ELFN1-AS1 promotes GC cell proliferation, migration, invasion, and EMT, and inhibits apoptosis by acting as a sponge for miR-211-3p and upregulating TRIM29 expression. Thus, the ELFN1-AS1/miR-211-3p/TRIM29 axis may be a potential target for GC treatment in the future.
Long noncoding RNA (lncRNA) extracellular leucine rich repeat and fibronectin type III domain containing 1-antisense RNA 1 (ELFN1-AS1) has been found to be upregulated in various tumors. However, the biological functions of ELFN1-AS1 in gastric cancer (GC) are not entirely understood. In the present study, the expression levels of ELFN1AS1, miR-211-3p, and TRIM29 are determined using reverse transcription-quantitative PCR. Subsequently, CCK8, EdU, and colony formation assays are performed to determine GC cell vitality. The migratory and invasive capabilities of GC cells are further evaluated using transwell invasion and cell scratch assays. Western blot analysis is performed to quantify the levels of proteins associated with GC cell apoptosis and epithelialmesenchymal transition (EMT). The competing endogenous RNA (ceRNA) activity of ELFN1-AS1 on TRIM29 through miR-211-3p is confirmed by pull-down, RIP, and luciferase reporter assays. Our study proves that ELFN1-AS1 and TRIM29 are highly expressed in GC tissues. ELFN1- AS1 silencing inhibits GC cell proliferation, migration, invasion and EMT, and induces cell apoptosis. Rescue experiments reveal that the oncogenicity of ELFN1-AS1 is modulated by acting as a sponge for miR-211-3p, thereby increasing the expression of the target gene of miR-211-3p, TRIM29. In summary, ELFN1-AS1 maintains GC cell tumorigenicity via the ELFN1-AS1/miR-211-3p/TRIM29 axis, indicating that this axis can be directed for GC treatment in the future.

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