LncRNA SNHG14 affects the malignant biological behaviors of hepatocellular carcinoma Huh7 cells via targeting the miR-579-3p/SPARC axis
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Abstract:
[Abstract] Objective: To investigate the effects of long non-coding RNA (lncRNA) small nucleolar RNA host gene 14 (SNHG14) on the malignant biological behavior of hepatocellular carcinoma (HCC) cells by targeting miR-579-3p/secreted protein acidic and rich in cysteine (SPARC) axis. Methods: Normal human hepatocytes (LO2) and HCC cells (Huh7, Hep3B, HepG2) were routinely cultured. Huh7 cells were randomly divided into control, sh-NC, sh-SNHG14, sh-SNHG14 + anti-NC, and sh-SNHG14 + anti-miR-579-3p groups. The mRNA expression levels of SNHG14, miR-579-3p, and SPARC in the above cells were detected by qPCR. Dual-luciferase reporter gene assay was applied to verify the regulatory relationship between SNHG14 and miR-579-3p, as well as between miR-579 3p and SPARC. The proliferation, migration, invasion, and apoptosis of Huh7 cells in each group were assessed using MTT, wound healing, Transwell, and flow cytometry assays, respectively. WB was used to detect the protein levels of PCNA, E-cadherin, vimentin, and SPARC. Results: In HCC cells, SNHG14 and SPARC mRNA were upregulated, whereas miR-579-3p was downregulated (all P < 0.05). There was a direct binding regulatory relationship between SNHG14 and miR-579-3p, as well as between miR-579-3p and SPARC mRNA (all P < 0.05). Knockdown of SNHG14 significantly inhibited the proliferation, migration, invasion, and the expression of PCNA and vimentin, as well as the mRNA and protein expression of SPARC in Huh7 cells (all P < 0.05), while promoting apoptosis, expression of miR-579-3p, and E-cadherin expression (all P < 0.05). Inhibition of miR-579-3p partially reversed the effects of SNHG14 knockdown on Huh7 cells (all P < 0.05). Conclusion: Knockdown of SNHG14 can inhibit the malignant biological behaviors of Huh7 cells and promote their apoptosis by targeting the miR-579-3p/SPARC axis. The SNHG14/miR-579-3p/SPARC axis may represent a potential therapeutic target for HCC.