Background: MicroRNA-628-3p (miR-628) has been reported to play important roles in the progression of multiple human cancer types. Nonetheless, whether the expression profile of miR-628 is altered in gastric cancer remains unclear and whether its aberrant expression plays a crucial part in the aggressiveness of gastric cancer is yet to be determined. Therefore, in this study, we systematically investigated the involvement of miR-628 in gastric cancer progression. Materials and methods: MiR-628 expression in gastric cancer tissues and cell lines were determined via reverse transcription-quantitative polymerase chain reaction (RT-qPCR). A CCK-8 assay, flow-cytometric analysis, Transwell assays, and a xenograft model experiment were performed to evaluate the influence of miR-628 overexpression on gastric cancer cells. Notably, the mechanisms underlying the tumor-suppressive activity of miR-628 in gastric cancer cells were explored by bioinformatics analysis, a luciferase reporter assay, RT-qPCR, and Western blotting. Results: MiR-628 expression was low in gastric cancer tissue samples and cell lines. The low expression of miR-628 was closely associated with the lymph node metastasis, invasive depth and TNM stage among patients with gastric cancer. Further clinical analysis indicated that patients with gastric cancer underexpressing miR-628 had a worse prognosis than did the patients with high miR-628 expression in the tumor. Overexpressed miR-628 restrained proliferation, migration, and invasion; induced apoptosis; and impaired tumor growth of gastric cancer cells. In addition, neuropilin 1 (NRP1) mRNA was validated as the direct target of miR-628 in gastric cancer. Long noncoding RNA small nucleolar RNA host gene 16 (SNHG16) was demonstrated to sponge miR-628 in gastric cancer. Moreover, miR-628 knockdown abrogated the influence of SNHG16 silencing on gastric cancer cells. Conclusion: Our findings elucidate how the SNHG16-miR-628-NRP1 pathway serves as a regulatory network playing crucial roles in gastric cancer progression, suggesting that this pathway may be a novel target of anticancer therapy.

Numerous studies have revealed that a subset of microRNAs (miRNAs) is aberrantly expressed in breast cancer. The dysregulation of miRNAs is involved in the tumorigenesis and progression of breast cancer due to their negative regulation of downstream target genes. Therefore, the identification of deregulated miRNAs in breast cancer may provide important insights into the diagnosis and treatment of patients with this disease. miRNA-511 (miR-511) has been identified to be deregulated in diverse human cancer types; however, neither the expression status nor the detailed roles of miR-511 in breast cancer have been clarified. Thus, it was aimed to determine the expression of miR-511 in breast cancer, examine the role in malignant progression and explore its downstream targets. The results of the present study revealed that the expression of miR-511 was downregulated in breast cancer tissues and cell lines. Decreased expression of miR-511 was significantly associated with lymph node metastasis and tumor stage in patients with breast cancer. Functional analyses revealed that restoring miR-511 expression suppressed breast cancer cell proliferation and colony formation, promoted apoptosis and reduced metastasis in vitro, while it attenuated tumor growth in vivo. Additionally, it was revealed that SRY-box 9 (SOX9) was a direct target gene of miR-511 in breast cancer cells. SOX9 was upregulated in breast cancer tissues and its expression was inversely correlated with that of miR-511. Furthermore, SOX9 inhibition simulated the tumor-suppressive roles of miR-511 overexpression in breast cancer cells, while SOX9 reintroduction partially rescued these effects of miR-511. Notably, the upregulation of miR-511 targeted SOX9 to deactivate the PI3K/Akt signaling in breast cancer in vitro and in vivo. In conclusion, miR-511 was downregulated in breast cancer, and impeded its malignant progression by directly targeting SOX9 and regulating the PI3K/Akt pathway. Thus, miR-511 is a potential therapeutic target in breast cancer.

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Background Recently, it has been reported that establishment of sister chromatid cohesion N-acetyltransferase 1 (ESCO1) is involved in tumorigenesis. However, its role in prostate cancer remains unclear. In the present study, the association between ESCO1 expression and the prognosis of prostate cancer was investigated, and the potential molecular mechanisms underlying its actions in tumor progression were also examined. Methods Immunohistochemical analysis was performed to detect the expression of ESCO1 in benign prostatic hyperplasia (BPH), human prostate cancer, and metastasis tissue samples, and the association between the establishment of ESCO1 expression and the prognosis of prostate cancer was investigated. The effect of ESCO1 expression on the viability, migration, and invasion of prostate cancer cells in vitro was analyzed, along with the effect of ESCO1 silencing on the growth of prostate tumors in vivo . Results The results demonstrated an increase in the expression of ESCO1 in prostate cancer tissue when compared with BPH, and it was significantly associated with tumor malignancy and poor patient survival. Additionally, knockdown of ESCO1 significantly inhibited the viability and migration of prostate cancer cell. Furthermore, we found that knockdown of ESCO1 significantly inhibited tumor growth in vivo . Pathway analysis identified that the silencing of ESCO1 significantly decreased the phosphorylation levels of protein kinase B. Conclusions The results of the present study indicate that ESCO1 plays a vital role in the progression of human prostate cancer; furthermore, ESCO1 may potentially serve as a prognostic marker and a novel therapeutic target for this disease.

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