Background: Prostate cancer (PCa) is a serious health threat for humans worldwide.Recent studies have revealed that microRNAs are associated with the progression of human cancers, including PCa. However, no study has been performed aiming to investigate the role of microNA-4286 (miR-4286) on PCa.Methods: A quantitative reverse transcriptase-polymerase chain reaction was conducted to analyze the expression level of miR-4286 in PCa cells. The connection of miR-4286 and spalt like transcription factor 1 (SALL1) was analyzed with a bioinformatic analysis tool, a dual-luciferase activity reporter assay and western blotting. The effects of miR-4286 and SALL1 on PCa cell behaviors were examined in vitro.Results: We showed miR-4286 expression was significantly increased in PCa cells compared to a normal cell line. Knockdown of miR-4286 could inhibit PCa cell proliferation but promote cell apoptosis by targeting SALL1.
Conclusions:The results of the present study suggest that miR-4286 overexpression represents a tumor promoter role in PCa.
Primary myelofibrosis (PMF) is a chronic myeloproliferative disorder in human bone marrow. Over 50% of patients with myelofibrosis have mutations in JAK2, MPL, or CALR. However, these mutations are rarely detected in children, suggesting a difference in the pathogenesis of childhood PMF. In this study, we investigated the response to drug treatment of a monozygotic twin pair with typical childhood PMF. The twin exhibited different clinical outcomes despite following the same treatment regimen. The transcriptomic profiles of patient samples after drug treatment (E2 and Y2) were significantly different between the twin pair, which is consistent with the observation that the drug treatment was effective only in the younger brother, despite the twin being genetically identical. Bioinformatics analysis of the drug-responsive genes showed that the JAK-STAT pathway was activated in the cured younger brother, which is opposite to the pathway inhibition observed in adult PMF cases following treatment. Moreover, apoptosis and cell cycle processes were both significantly influenced by drug treatment in the sample of younger brother (Y2), implying their potential association with the pathogenesis of childhood PMF. Gene mutations in JAK2, MPL, or CALR were not observed; however, mutations in genes including SRSF2 and SF3B1 occurred in this twin pair with childhood PMF. Gene fusion events were extensively screened in the twin pair samples and the occurrence of IGLV2-14-IGLL5 gene fusion was confirmed. The current study reported at transcriptomic level the different responses of monozygotic twin brothers with childhood PMF to the same androgen/prednisone treatment regimen providing new insights into the potential pathogenesis of childhood PMF for further research and clinical applications.
This paper proposes a new navigation modulation based on orthogonal frequency division multiplexing (OFDM). We derived the autocorrelation function and power spectral density of the OFDM modulation. The influence of the cyclic prefix and zero-padding is discussed. The influence of OFDM modulation parameters on navigation signal performance was deeply analyzed, which can help signal designers choose the OFDM parameters. The main peak of the proposed autocorrelation function is narrow and has good tracking accuracy. The sidelobe is lower, and the delay locking loop is more robust. The power spectrum density is evenly distributed in the main lobe of the signal, and the anti-interference is good. By comparing OFDM navigation signals with other navigation signals, it can be found that OFDM navigation signals have good tracking accuracy and a strong anti-interference ability. Combined with the proposed navigation modulation and communication signal, the OFDM navigation signal has a low bit error rate for the communication signal and has a good communication integration potential, which can meet the business requirements of the future communication and navigation integration market.
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