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A large number of studies in China and other countries have confirmed that circularHIPK3 (circHIPK3) plays an important role in the pathophysiological processes of various diseases. Through the action of sponge miRNA (miR), circHIPK3 regulates cell proliferation, differentiation, and migration, and plays a key role in disease processes. By referring to a large number of research reports, this article explores the specific functional role of circHIPK3 in fibrotic diseases, cancer, and other diseases. This review aims to clarify the role of circHIPK3 in disease processes in order to aid further studies into the specific pathogenesis and clinical diagnosis of various diseases and provide new ideas for treatments.

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The effect of atmosphere on the fabrication of boronized Ti6Al4V/hydroxyapatite (HA) composites was investigated by microwave sintering of the mixture of Ti6Al4V alloy, HA, and TiB 2 powders at 1050 °C for 30 min in the mixed gases of Ar + N 2 , Ar + CO, and Ar + H 2 , respectively. The presence of N 2 , CO, and H 2 in the atmosphere caused formations of TiN, TiC, and TiH 2 in the composites, respectively, together with evident microstructural changes that determined the mechanical properties (compressive strength, compressive modulus, and Vickers microhardness) and wettabilities of the composites after sintering. It was found that the composite exhibited the best mechanical performance with compressive strength of 148.59 MPa, compressive modulus of 13.9 GPa, and Vickers microhardness of 300.39 HV by microwave sintering in the mixed gas of Ar + H 2 , followed by those obtained in the mixed gases of Ar + N 2 and Ar + CO. All of the composites possessed desirable wettabilities, irrespective of the sintering atmosphere, as demonstrated by their very low water contact angles (≤31.9°). The results indicated that it is critical to control the extents of nitration and carbonization for maintaining the performance of the composites, especially the mechanical properties, whereas there is no strict requirement for the same objective using the mixed gas of Ar + H 2 in which qualified composites could be obtained for implant applications.

Epithelial–mesenchymal transition (EMT) is closely correlated to metastasis formation generation and maintenance of cancer stem cells, nevertheless, the underlying mechanisms are unclear. The aim of this study is to investigate the role of maternal embryonic leucine-zipper kinase (MELK) in EMT regulation in oral squamous cell carcinoma (OSCC). We found that there was overexpression of MELK in human OSCC tissues, and high MELK expression was correlated with lymphatic metastasis and led to poor prognosis in patients with OSCC. We also confirmed that MELK is closely correlated to the EMT process using a human OSCC tissue microarray. Additionally, MELK expression was observed to be regulated in several OSCC cell lines, and knockdown of MELK genes inhibited cell proliferation, migration, invasion and EMT of OSCC cells in vitro . Furthermore, silencing of MELK suppressed tumour growth in vivo , and experimental research verified that MELK may augment OSCC development via mediating the Wnt/Notch signalling pathway. Our findings suggest that MELK serves as an oncogene to improve malignant development of OSCC via enhancing EMT, and MELK might be a potential target for anticancer therapeutic.

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Recent studies have demonstrated an important role for mitotically associated long non-coding RNA (MANCR) in carcinogenesis and cancer progression, but its function has not been elucidated in head and neck squamous cell carcinoma (HNSCC). In this study, we identified differentially expressed MANCR from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases across 24 cancer types and included 546 HNSCC patients. Furthermore, high expression of MANCR was verified in HNSCC cell lines and tissue by using real-time quantitative PCR (RT-qPCR) analysis. The Kaplan–Meier analysis showed a worse prognosis with higher levels of MANCR for HNSCC. The univariate Cox regression and multivariate Cox regression analyses revealed that MANCR was a high-risk factor in patients with HNSCC. Thereafter, we carried out the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. It was indicated that MANCR participates in axonogenesis and ECM-receptor interaction. Further enrichment analysis demonstrated that the expression of MANCR was positively correlated with the T gamma delta (tgd) cells, neutrophils, and Th1 cells, and negatively correlated with the infiltration of B cells, CD8 T cells, and T cells in HNSCC. In addition, in vitro experiments showed that knockdown of MANCR in HNSCC cells markedly inhibited cell proliferation, migration, and invasion. We find that MANCR was elevated in HNSCC and promoted the malignant progression of HNSCC. MANCR may serve as a potential biomarker in prognostic implications for HNSCC patients. The positive correlation between MANCR and immune infiltration cells may provide novel therapeutic targets and personalized immune-based cancer therapy for HNSCC.

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