Multiple myeloma (MM) is a clonal plasma cell disorder which constitutes the second most common hematological malignancy, and remains an incurable tumor with poor survival. Recently, interleukin-17 (IL-17), produced locally in the tumor microenvironment, has been reported to play a crucial role in tumor immunity. In this study, we determined that exposure of MM cells to IL-17 had various promotive influences on different aspects of tumor progression. IL-17 significantly induced cell proliferation, inhibited cellular apoptosis, repressed cell adhesion to fibronectin and collagen I, and facilitated cell migration. Exposure to IL-17 also resulted in epithelial-mesenchymal transition (EMT), as evidenced by repression of the epithelial marker E-cadherin, and induction of the mesenchymal marker Vimentin, and EMT transcription factors Snail and Slug. Further experiments showed that IL-17 activated the oncogenic p65 transcription factor, which directly repressed the miR-192 gene via binding to the miR-192 promoter. Loss of miR-192 in MM cells can mimic the effects of IL-17, and was required for the above oncogenic effects of IL-17 on MM. Furthermore, we found that miR-192, and its homologous miR-215 directly targeted the 3′-untranslated regions of IL-17Rs, including IL-17RA and RE mRNA. By examining bone marrow specimens derived from MM patients, a negative correlation between miR-192 expression and IL-17 or IL-17RA expression was observed. Also, IL-17 was negatively correlated with E-cadherin and positively with Vimentin. Taken together, our study provides evidence that the IL-17/miR-192/IL-17Rs regulatory feedback loop is manifest in MM and might represent a promising and efficient prognostic marker and therapeutic target for MM.

This review describes for the first time the role played by electrochemical biosensors in SARS-CoV-2 detection from a bibliometric perspective.

Burkitt lymphoma (BL) has a high mortality rate and its treatment is currently limited to chemotherapy combined with immunotherapy. The long non-coding RNA antisense non-coding RNA in the INK4 locus (ANRIL) has been identified as an oncogene that can regulate cell proliferation and apoptosis in multiple types of cancer. However, the function of ANRIL in BL remains unknown. The present study aimed to determine the effect of ANRIL on cell proliferation and apoptosis in BL. Reverse transcription-quantitative PCR was used to analyze the expression levels of ANRIL in BL cells. The effect of ANRIL knockdown on BL cells was determined using Cell Counting Kit-8, flow cytometric, western blotting, immunofluorescence staining and Hoechst staining assays. The results revealed that ANRIL silencing inhibited the proliferation and promoted the apoptosis of BL cells. In addition, the expression levels of cyclin D1, E2F transcription factor 1 and Bcl-2 were downregulated, while the expression levels of cyclin-dependent kinase inhibitor 1A, Bcl-2-associated X protein, cleaved-caspase-9/pro-caspase-9 and cleaved-caspase-3/pro-caspase-3 were upregulated. Furthermore, the knockdown of ANRIL activated the TGF-β1 signaling pathway, as evidenced by the upregulated expression levels of TGF-β1, phosphorylated (p)-SMAD2/3/SMAD2/3, p-SMAD1/SMAD1 and sphingosine-1-phosphate receptor 2. Moreover, the protective effect of ANRIL silencing in BL could be inhibited by the TGF-β receptor type I/II dual inhibitor, LY2109761. In conclusion, the findings of the present study suggested that the knockdown of ANRIL may inhibit cell proliferation and promote cell apoptosis in BL by regulating the TGF-β1 signaling pathway, which may provide a novel target for the treatment of BL.

The objective of this study was to investigate the expression and significance of the transforming growth factor β type II receptor (TGFβRII) in diffuse large B cell lymphoma. All patients were enrolled at the First Affiliated Hospital of Liaoning Medical University between 2001 and 2007. The median follow-up period was 53.3 months. Of the 338 patients studied, 131 (38.76 %) had TGFβRII positive expression on immunohistochemistry. The 5 year survival rate was significantly higher in patients with TGFβRII expression than in those without TGFβRII expression (40.3 vs. 31.6 %, P = 0.041). Multivariate analysis identified TGFβRII expression as an independent predictive parameter for survival, in addition to lactate dehydrogenase, clinical stage, and histologic subtype. TGFβRII expression may be considered a new prognostic factor of diffuse large B cell lymphoma.