[The mechanism of HOTAIR regulating the proliferation and apoptosis of prostate cancer cells by targeting down-regulation of miR-152 to improve the expression of FOXR2].

Objective: To clarify the effect of FOXR2 on the proliferation and apoptosis of prostate cancer cells and to reveal the mechanism. Methods: The expression of FOXR2 in clinical samples of prostate cancer were detected by Quantitative Real-time PCR (qRT-PCR) and Western blotting. The CCK8 proliferation kit and the Annexin V-FITC apoptosis kit, flow cytometry were used to detect the proliferation and apoptosis of prostate cancer cells with or without the FOXR2 knockdown. Combined with the results of microRNA chip, we predicted the related miR-152 and detected the relationship between miR-152 and FOXR2 by luciferase reporter gene assay. The correlation between HOTAIR and miR-152 is clearly defined by software prediction and qRT-PCR. Results: FOXR2 had a relatively high expression in the prostate cancer tissue.The mRNA expression of FOXR2 is 4.9 times that of adjacent tissues, and the protein level was also significantly up-regulated. In the PC3 cell line, the specific knock-down of FOXR2 inhibits the proliferation of cells and promotes cell apoptosis. According to the microRNA chip results and luciferase reporter gene assay, we found miR-152 could regulate the expression of FOXR2; and FOXR2 3 'UTR had two miR-152 binding sites, all of which could control the expression of FOXR2. The results of LNCediting and qRT-PCR suggest that HOTAIR is negatively correlated with the expression of miR-152, and is involved in the regulation of miR-152 expression in prostate cancer. Conclusion: FOXR2 up-regulation can promote the proliferation and inhibit the apoptosis of prostate cancer cells because that HOTAIR restrains the expression of miR-152.

Inhibition of miR-221 influences bladder cancer cell proliferation and apoptosis.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Inhibition of miR-221 influences bladder cancer cell proliferation and apoptosis, by H. Liu, J.-K. Chang, J.-Q. Hou, Z.-H. Zhao, L.-D. Zhang, published in Eur Rev Med Pharmacol Sci 2017; 21 (14): 3193-3199-PMID: 28770966" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/13140.

Inhibition of miR-221 influences bladder cancer cell proliferation and apoptosis.

OBJECTIVE: Janus kinase (JAK) - signal transducer and activator of transcription (STAT) signaling pathway participate in cell proliferation and apoptosis. Suppressors of cytokine signaling 3 (SOCS3) are negative regulators of JAK-STAT3. SOCS3 was found significantly declined, while microRNA-221 (miR-221) obviously up-regulated in bladder cancer tissue. Bioinformatics analysis revealed the complementary binding site between miR-221 and 3'-UTR of SOCS3. This study investigated the role of miR-221 in regulating SOCS3/JAK-STAT3 signaling pathway and bladder cancer cell proliferation and apoptosis. PATIENTS AND METHODS: Bladder cancer tumor tissue and para-carcinoma tissue were collected from patients to test miR-221 and SOCS3 expressions. Dual luciferase assay was used to test the targeting regulatory effect of miR-221 on SOCS3. MiR-221, SOCS3, p-JAK1, p-JAK2, and survivin expressions were compared in T24 and HBEC cells. T24 cells were divided into miR-NC, miR-221 inhibitor, pSicoR-blank, pSicoR-SOCS3, and miR-221 inhibitor + pSicoR-SOCS3 groups. Flow cytometry was applied to detect cell apoptosis. EdU staining was adopted to evaluate cell proliferation. RESULTS: MiR-221 significantly increased, while SOCS3 obviously reduced in bladder cancer tissue compared with para-carcinoma tissue. MiR-221 targeted inhibited SOCS3 expression. MiR-221, phosphorylated JAK1 (p-JAK1), phosphorylated JAK2 (p-JAK2), phosphorylated STAT3 (p-STAT3), and survivin levels markedly up-regulated, whereas SOCS3 expression apparently declined in T24 cells compared with that in HBEC cells. MiR-221 inhibitor and/or pSicoR-SOCS3 elevated SOCS3 expression, decreased p-JAK1, p-JAK2, p-STAT3, and survivin levels, enhanced cell apoptosis, and attenuated cell proliferation. CONCLUSIONS: MiR-221 elevated, while SOCS3 reduced in bladder cancer tissue. Inhibition of miR-221 suppressed T24 cell proliferation and induced apoptosis by up-regulating SOCS3 expression, lowering JAK-STAT3 signaling pathway activity, and attenuating survivin expression.

Induction of metalloelastase mRNA in murine peritoneal macrophages by diethylmaleate.

Macrophage-specific metalloelastase (MME) hydrolyzes elastin and other matrix proteins and plays an important physiological role in tissue remodeling and pathological tissue destruction. We have examined the effects of diethylmaleate (DEM), an electrophilic agent that reacts with sulfhydryls, on the expression of MME mRNA in mouse peritoneal macrophages. Quantification of MME mRNA by Northern blot analysis revealed that basal mRNA levels were quite low in freshly isolated cells, although mRNA levels increased markedly and reached a steady level within 12 h when cells were cultured in a serum-supplemented RPMI 1640 medium. When macrophages were challenged with DEM at 0.05-1.0 mM for 8 h the expression of the MME gene was enhanced further. In the presence of 0.1 mM DEM, the level of the MME mRNA increased 2-fold compared to the control levels after 6-9 h and decreased to control levels in 24 h. Other electrophilic agents, catechol and 1-chloro-2,4-dinitrobenzene, also enhanced MME gene expression. However, oxidative stress agents such as hydrogen peroxide, menadione, paraquat (an O-2 generator), sodium arsenite and cadmium chloride had no effect on MME gene expression. These results indicate that the electrophilic agents selectively enhance the expression of MME mRNA during primary culture of the macrophages.

Characterization and application of three novel monoclonal antibodies against human 4-1BB: distinct epitopes of human 4-1BB on lung tumor cells and immune cells.

4-1BB, a member of the tumor necrosis factor receptor (TNFR) superfamily, is a costimulatory receptor that is primarily expressed on activated T cells and professional antigen-presenting cells. In this study, the expression pattern of 4-1BB on immunology cells and tumor cells was explored by flow cytometry using newly generated three anti-4-1BB monoclonal antibodies (mAbs; 6F9, 7D6, and 1G11), which bind to distinct 4-1BB epitopes. Compared with the available 4-1BB mAb 4B4-1 that recognized 4-1BB on activated T cells and monocytes, the novel mAbs also could recognize 4-1BB on some cancer cell lines, particularly on lung cancer cell lines such as SPC-A-1, H446, H460, and H1299 by flow cytometry analysis, western blot, and RT-PCR. Immunohistochemistry staining showed the 4-1BB was expressed on lung tumor tissue (33/35) but not on normal lung tissue (3/3). It was determined that 4-1BB was strictly expressed on lung cancer cells, which may provide information on the 4-1BB signal in tumor immunology mechanism.