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microRNA‑188 (miR‑188) acts as a tumor suppressor in various types of human cancer, including glioma, oral squamous cell carcinoma and hepatocellular carcinoma. However, the function and mechanism of miR‑188 in pediatric osteosarcoma (OS) have yet to be investigated. In the present study reverse transcription‑quantitative polymerase chain reaction revealed that miR‑188 expression was significantly downregulated in pediatric OS tissues and cell lines. miR‑188 overexpression markedly suppressed OS cell proliferation, migration and invasion, and induced cellular apoptosis. An in vivo assay demonstrated that miR‑188 overexpression inhibited tumor growth. miR‑188 targeted SOX4 to regulate its expression. miR‑188 expression was inversely correlated with SOX4 in pediatric OS tissues. SOX4 restoration abrogated the inhibitory effects of miR‑188 on OS cells. The results of the present study indicated that miR‑188 suppressed pediatric OS progression by targeting SOX4.

Esophageal cancer (EC) is one of the most common gastrointestinal cancers, which leads to the sixth ranking of cancer-related death. Long non-coding RNAs (lncRNAs) play pivotal roles in many biological processes. lncRNA human urothelial carcinoma associated 1 (UCA1) is significantly upregulated and functions as an important oncogene in many types of human cancers. However, the role of UCA1 in EC and its underlying mechanism remains unclear. In the present study, we demonstrated that UCA1 was significantly upregulated in EC tissues and associated with poor prognosis. Overexpression of UCA1 promoted the proliferation of EC cells, while silence of UCA1 inhibited EC cells growth. Furthermore, we found that Sox4 was a direct target gene of UCA1. UCA1 regulated Sox4 expression through functioning as a competing endogenous RNA (ceRNA). UCA1 directly interacted with miR-204 and decreased the binding of miR-204 to Sox4 3'UTR, which suppressed the degradation of Sox4 mRNA by miR-204. This study provides the first evidence that UCA1 promotes cell proliferation through Sox4 in EC, suggesting that UCA1 and Sox4 may be potential therapeutic targets for EC.

Increasing evidence has confirmed that dysregulation of microRNAs (miRNAs) can contribute to the progression and metastasis of human tumors. Previous studies have shown that dysregulation of microRNAs (miRNAs) can contribute to the progression and metastasis of human tumors. However, the precise mechanisms of miR‑132 in osteosarcoma have not been well clarified. Real-time PCR was performed to detect the expression of miR‑132 in osteosarcoma cell lines. miR-132 mimic, miR‑132 inhibitor and negative control were transfected into osteosarcoma cells and the effects of miR‑132 on the cell growth and metastasis were investigated. Furthermore, protein level of Sox4 was measured by western blotting. Luciferase assays were performed to validate Sox4 as miR‑132 target in osteosarcoma cells. We found that miR‑132 was downregulated in osteosarcoma cell lines. Introduction of miR‑132 significantly inhibited proliferation, arrested cell cycle and induced apoptosis in osteosarcoma cells. Besides, invasion and epithelial-mesenchymal transition (EMT) of osteosarcoma cells was suppressed by overexpressing miR‑132. However, downregulation of miR‑132 promoted cell growth and metastasis in osteosarcoma cells. Bioinformatics analysis predicted that Sox4 was a potential target gene of miR‑132. Luciferase reporter assay demonstrated that miR‑132 could directly target Sox4. Moreover, the low level of miR‑132 was associated with increased expression of Sox4 in osteosarcoma cells. Sox4 inhibition suppressed cell malignant behaviors. Overexpression of Sox4 in osteosarcoma cells transfected with miR‑132 mimic partially reversed the inhibitory effect of miR‑132. In conclusion, miR‑132 inhibited cell growth and metastasis in osteosarcoma cells by downregulation of Sox4, and knockdown of Sox4 was essential for the miR-132-inhibited cell growth and metastasis in osteosarcoma cells.

SOX genes play an important role in a number of developmental processes. The transcription factor SOX11 is one of the members of the SOX family emerging as important transcriptional regulators. The aim of this study was to investigate the role of SOX11 in prostate cancer (PCa) and its expression pattern and clinical significance. The gene expression of SOX11 in human PCa tissues compared with benign prostate hyperplasia (BPH) tissues was detected using real-time quantitative reverse transcriptase-polymerase chain reaction (QRT-PCR) analysis and immunohositochemistry. SOX11 overexpression cell model was used to examine the role of SOX11 in cell growth and metastasis in vitro. The results showed that the positive rate of SOX11 staining was 16.67 % (10/60) in cases of prostatic carcinoma and 81.67 % (49/60) in cases of BPH, and the difference of SOX11 expression between PCa and BPH was statistically significant (P < 0.001). SOX11 mRNA level was lowly expressed in PCa cell lines compared to RWPE-1. SOX11 overexpression suppresses PCa cell migration and invasion. In conclusion, our findings demonstrate that SOX11 could suppress cell proliferation, migration, and invasion of PCa in vitro.