miR-5089-5p suppresses castration-resistant prostate cancer resistance to enzalutamide and metastasis via miR-5089-5p/SPINK1/ MAPK/MMP9 signaling.

Whether serine protease inhibitor Kazal type 1 (SPINK1) being associated with enzalutamide (Enz) resistance and metastasis of castration-resistant prostate cancer (CRPC) has not been clear. SPINK1 promoted Enz resistance by upregulating Androgen receptor splicing variant 7 (ARv7), and enhanced the invasion/migration of Enz-resistant cells via ERK/p38/ MMP9 signaling. Furthermore, miR-5089-5p suppressed SPINK1 mRNA through direct binding to its 3'UTR, and reversed its pro-proliferative and pro-metastatic effects. Mice bearing SPINK1-knockdown Enz-resistant PCa tumors showed significantly longer survival compared with those bearing wild-type tumors, while treatment with miR-5089-5p inhibitor abrogated the protective effects of SPINK1 knockdown. Taken together, SPINK1 can be used as a biomarker of resistance to Enz, and the miR-5089-5p/SPINK1/MAPK/MMP9 axis is a suitable therapeutic target against Enz-resistant and metastatic CRPC.Methods: The expression of SPINK1 in Enz-resistant prostate cancer (PCa) cell lines was detected through next-generation sequencing data and metastatic PCa patients. In vivo and in vitro experiments were performed to investigate the role of SPINK1 in Enz-resistance and metastasis.

Adaptive Rate-Compatible Non-Binary LDPC Coding Scheme for the B5G Mobile System.

This paper studies an adaptive coding scheme for B5G (beyond 5th generation) mobile system-enhanced transmission technology. Different from the existing works, the authors develop a class of rate-compatible, non-binary, low-density parity check (RC-NB-LDPC) codes, which expresses the strong connection between the algebra-based and graph-theoretic-based constructions. The constructed codes can not only express rate-compatible (RC) features, but also possess a quasi-cyclic (QC) structure that facilitates the encoding implementation. Further, in order to achieve the code rate-adaptive allocation scheme, the authors propose using the K-means++ clustering algorithm to cluster different channel environments, considering various factors that affect channel characteristics. Finally, in order to present the advantages of the adaptive coding scheme, the authors construct a coding scheme for image transmission. The numerical results demonstrate that the developed code can obtain better waterfall performance in a larger code rate range, which is more suitable for data transmission; the adaptive coding transmission scheme can obtain higher reconstructed image quality compared to the fixed code rate-coding scheme. Moreover, when considering unequal error protection (UEP), the proposed scheme can further improve the reconstructed image quality.

[Macrophage migration-inhibitory factors expression and its effects on proliferation in human dental pulps].

OBJECTIVE: To investigate the expression of macrophage migration-inhibitory factors (MIF) in clinically healthy and inflamed human pulp tissues and the effects of rhMIF on the proliferation of human dental pulp cells (HDPC). METHODS: Immunohistochemistry was used to detect the localization of MIF expression in clinically healthy pulp and inflamed pulp tissues. Quantitative real-time polymerase chain reaction (PCR) was performed to evaluate the mRNA levels of MIF in pulp specimens. In addition, the culture supernatants of HDPC were collected after HDPC was stimulated by lipopolysaccharide (LPS) for 24 h, and then the MIF levels were assayed by quantitative sandwich enzyme-linked immunosorbent assay. Meanwhile, the effects of rhMIF on the proliferation of HDPC at different concentrations for 24 and 48 h were observed by cell counting kit-8 (CCK-8). RESULTS: MIF was mainly distributed in odontoblasts of healthy pulp tissue, however, in inflamed pulp tissue, it was widely detected in fibroblasts, inflammatory infiltrates and endothelial cells as well as odontoblasts. Quantitative real-time PCR showed that there was no significant difference in MIF mRNA levels between inflamed pulps and healthy pulps (P > 0.05). Additionally, the secretion of MIF was significantly increased by stimulation with LPS at the concentration of 0.1 and 1.0 mg/L [(1772.58 ± 495.05), (1692.58 ± 337.45) ng/L] (P < 0.05), and the concentration was (1048.53 ± 161.81) ng/L in control group. rhMIF stimulated the HDPC's proliferation at the concentration of 10, 30, 60 µg/L for 24 and 48 h. CONCLUSIONS: MIF was expressed in pulp tissue and its expression was increased after stimulation by LPS. rhMIF increased the proliferation of HDPC. These results suggest that MIF may be involved in the process of pulpal inflammation.