ArticleMolecular biology reports2023
The siRNA-mediated knockdown of SNHG4 efficiently induced pro-apoptotic signaling and suppressed metastasis in SW1116 colorectal cancer cell line.
Article in Molecular biology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 7 citations in OpenAlex.
- Unraveling the role of long non-coding RNAs in therapeutic resistance in acute myeloid leukemia: New prospects & challenges.Non-coding RNA research · 2024Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLong non-coding RNAs are broadly dysregulated in disease conditions, especially cancer, and are associated with tumor initiation, invasion, and overall survival. This study aimed to elucidate the expression level of Small Nucleolar RNA Host Gene 4 (SNHG4) lncRNA in colorectal cancer (CRC) and its effect on cell cycle progression, invasion, and death. METHODS AND
resultsWe evaluated the expression level of SNHG4 in clinical samples, including CRC tissues, adenomatous colorectal polyps (ACP), and their marginals. SNHG4-silenced SW1116 cells were used to evaluate the cell viability, cycle arrest, invasion, and apoptosis using MTT assay, scratching, flow cytometry, and immunoblotting. We also predicted molecular networks related to the SNHG4 involvement in CRC development. Results showed that SNHG4 expresses in cancerous tissues significantly higher than in polyps and marginals. This overexpression discriminated CRC from marginals and ACP with a suitable prognostic potential. Silencing of SNHG4 arrested the cell cycle at S and G2 phases and promoted early apoptosis in SW1116. It affected the active form of MMP2 and prevented cell invasion. Sponging of miRNAs which promotes the choline metabolism is the probable mechanism of SNHG4 involvement in CRC.
conclusionsIn conclusion, SNHG4 promotes CRC by dysregulating apoptosis and cell migration, and shows significant prognostic potential for CRC.
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