As a member of the S100 protein family, S100A11 expression is often upregulated in human cancer tissues. Numerous studies have demonstrated that S100A11 plays an important role in the progression of cancer. However, the function of S100A11 in ovarian cancer remains elusive. In the present study, the expression levels of S100A11 were found to be significantly increased in ovarian cancer cells. Subsequently, the expression of S100A11 in ovarian cancer HO8910 cells was knocked down using short hairpin (sh)RNA in order to investigate the biological effects of S100A11 on the progression of the disease. The results demonstrated that knockdown of S100A11 by shRNA inhibited the proliferation, anchorage-independent growth, invasion and migration of HO8910 cells. In addition, knockdown of S100A11 increased the expression of E-cadherin and decreased the expression of Snail in HO8910 cells. Collectively, these results indicated that S100A11 was able to promote the growth, invasion and migration of ovarian cancer cells. Therefore, S100A11 may serve as a potential molecular target for the diagnosis and treatment of ovarian cancer.

The use of corticosteroids has been controversial in viral pneumonia. In most cases, application of methylprednisolone in severe and critical viral pneumonia patients can quickly alleviate the symptoms of dyspnea and prevent disease progression. However, some scholars have confirmed that corticosteroids delayed the body's clearance of the virus. In our retrospective non-randomized study, 34 patients under 50 years old and diagnosed with coronavirus disease 2019 (COVID-19) were included. According to the given methylprednisolone treatment (n = 18) or not (n = 16), they were separated into two groups. By comparing the clinical data we concluded that corticosteroids therapy can effectively release COVID-19 symptoms such as persistent fever and difficult in breathing, improve oxygenation, and prevent disease progression. However, it can prolong the negative conversion of nucleic acids.

BackgroundmiR-19 is a critical carcinogenic miRNA that participates in important biological processes of human malignancies. CBX7 plays a key role in lung cancer development and progression. In the present study, for the first time, we investigated the correlation between miR-19 and CBX7 in non-small-cell lung cancer (NSCLC).MethodsmiR-19 expression in NSCLC tissues and lung cancer cell lines was detected using quantitative reverse transcriptase PCR (qRT-PCR). Luciferase reporter assay, qRT-PCR, Western blot, and immunohistochemical assay were conducted to identify the target reaction of miR-19 and CBX7. Moreover, the influence of miR-19 on lung cancer cell proliferation, migration, and invasion was studied including cell counting kit-8 assay, scratch assay, transwell assay, flow cytometry assay, and staining assays.ResultsmiR-19 was overexpressed in NSCLC tissues and lung cancer cell lines. Luciferase reporter assay demonstrated that miR-19 could inhibit CBX7 expression via binding to the 3′-UTR of CBX7. Furthermore, miR-19 remarkably decreased CBX7 protein and mRNA expression. Additionally, overexpression of miR-19 could significantly enhance lung cancer cell proliferation and migration.ConclusionmiR-19 functions as a tumor accelerator promoting lung cancer cell proliferation through targeting CBX7 and inhibiting its expression.

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