Introduction: Studies have found that Lnc-HCG11 is an important regulator of cancer. However, the function of Lnc-HCG11 in NSCLC is not known. Therefore, this experimental design was based on Lnc-HCG11 to explore the pathogenesis of NSCLC.
Methods: RT-qPCR was used to detect the expression of Lnc-HCG11 and miR-224-3p in NSCLC. The effects of Lnc-HCG11 and miR-224-3p on proliferation and apoptosis of NSCLC cells were detected by CCK-8 assay, Edu assay and Annexin V-FITC/PI assay. Target gene prediction and screening, luciferase reporter assays were used to verify downstream target genes for lnc-HCG11 and miR-224-3p. Western blotting was used to detect the protein expression of caspase-3. The tumor changes in mice were detected by in vivo.
Results: Lnc-HCG11 was significantly reduced in NSCLC. Lnc-HCG11 significantly inhibited cell proliferation of NSCLC cells and induced apoptosis. miR-224-3p was significantly elevated in the NSCLC cell line. Moreover, miR-224-3p significantly increased cell proliferation and inhibited apoptosis of NSCLC cells. Furthermore, Lnc-HCG11 was negatively correlated with miR-224-3p expression. Lnc-HCG11 over-expression was up-regulated the expression levels of c-caspase-3 and caspase-3. Finally, the results of in vivo animal models confirmed that Lnc-HCG11 inhibited tumor growth by modulating the miR-224-3p/c-caspase-3 axis.
Conclusion: Lnc-HCG11 could inhibit the progression of NSCLC by modulating the miR-224-3p/caspase-3 axis, and Lnc-HCG11 may be a potential therapeutic target for NSCLC.
Keywords: Lnc-HCG11, miR-224-3p, non-small-cell lung cancer, proliferation, apoptosis