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Sall4 is a novel oncogene found upregulated in several malignancies including colon cancer. However, its upstream regulatory miRNA is still undefined. miR-219-5p is regarded as a tumor-related miRNA in cancer research. Nevertheless, its actual role of whether inhibiting or promoting tumorigenesis is unclear in colon cancer. Potential interaction between Sall4 and miR-219-5p is predicted by TargetScan. CCK-8 test was used for evaluation of cell proliferation and cell survival rates. Western blot analysis and real-time PCR were applied for detection of target molecules. Luciferase assay was a direct confirmation of mutual interaction. Wound healing assay and transwell assay were conducted for cell migration and invasion tests. Flow cytometry was used for cell apoptosis analysis. Tissue specimens and cell lines were explored for miR-219-5p inhibition on colon cancer proliferation, migration, invasion, apoptosis and drug resistance by targeting Sall4. The results show that miR-219-5p inhibited carcinogenesis of colon cancer by targeting oncogene Sall4.

Osteosarcoma (OS) is a rare malignant bone tumor that commonly occurs in children and adolescents and causes pain and swelling of the long bones of the legs and arms. Long non-coding RNA (lncRNA) and micro (mi)RNA-101 are important in the initialization and progression of OS. However, the mechanism underlying the role of the lncRNA and miRNA-101 in OS remains to be fully elucidated. In the present study, through reverse transcription-quantitative polymerase chain reaction analysis, it was first found that the lncRNA SNHG1 was upregulated and miRNA-101-3p was downregulated in OS tissues and cell lines. Second, the knockdown of lncRNA SNHG1 induced cell apoptosis and maintained the cell cycle at the G0/G1 phase, which decreased the overall cell viability. Furthermore, according to a dual-luciferase assay and western blot analysis, miRNA-101-3p was found to be a target of the lncRNA SNHG1 in OS, which further regulated the expression of Rho-associated coiled-coil-containing protein kinase 1 (ROCK1). It was found that the phosphoinositide 3-kinase/ATK pathway was inactivated and that epithelial-mesenchymal transition was activated in OS cell lines with overexpression of the lncRNA SNHG1. Taken together, in OS cell lines, the lncRNA SNHG1 acted as an oncogene, and miRNA-101-3p was considered a tumor suppressor. The lncRNA SNHG1 promoted OS cell proliferation, migration and invasion by downregulating the expression of miRNA-101-3p, which enhanced the expression of ROCK1.