Long noncoding RNAs (lncRNAs) play important roles in regulating the development and progression of many cancers. However, the clinical significance of specific lncRNAs in the context of nasopharyngeal carcinoma (NPC) and the molecular mechanisms by which they regulate this form of cancer remain largely unclear. In this study we found that the lncRNA PVT1 was upregulated in NPC, and that in patients this upregulation was associated with reduced survival. RNA sequencing revealed that PVT1 was responsible for regulating NPC cell proliferation and for controlling a hypoxia-related phenotype in these cells. PVT1 knockdown reduced NPC cell proliferation, colony formation, and tumorigenesis in a subcutaneous mouse xenograft model systems. We further found that PVT1 serves as a scaffold for the chromatin modification factor KAT2A, which mediates histone 3 lysine 9 acetylation (H3K9), recruiting the nuclear receptor binding protein TIF1β to activate NF90 transcription, thereby increasing HIF-1α stability and promoting a malignant phenotype in NPC cells. Overexpression of NF90 or HIF-1α restored the proliferation in cells that had ceased proliferating due to PVT1 or KAT2A depletion. Conversely, overexpression of active KAT2A or TIF1β, but not of KAT2A acetyltransferase activity-deficient mutants or TIF1β isoforms lacking H3K9ac binding sites, promoted a PVT1-mediated increase in NF90 transcription, as well as increased HIF-1α stability and cell proliferation. PVT1 knockdown enhanced the radiosensitization effect in NPC cells via inhibiting binding between H3K9ac and TIF1β in a manner. Taken together, our results demonstrate that PVT1 serves an oncogenic role and plays an important role in radiosensitivity in malignant NPC via activating the KAT2A acetyltransferase and stabilizing HIF-1α.

To realize unmanned pose detection of a coalmine boom-type roadheader, an ultra-wideband (UWB) pose detection system (UPDS) for a roadheader is designed, which consists of four UWB positioning base stations and three roadheader positioning nodes. The positioning base stations are used in turn to locate the positioning nodes of the roadheader fuselage. Using 12 sets of distance measurement information, a time-of-arrival (TOA) positioning model is established to calculate the 3D coordinates of three positioning nodes of the roadheader fuselage, and the three attitude angles (heading, pitch, and roll angles) of the roadheader fuselage are solved. A range accuracy experiment of a UWB P440 module was carried out in a narrow and closed tunnel, and the experiment data show that the mean error and standard deviation of the module can reach below 2 cm. Based on the TOA positioning model of the UPDS, we propose a fusion-positioning algorithm based on a Caffery transform and Taylor series expansion (CTFPA). We derived the complete calculation process, designed a flowchart, and carried out a simulation of CTFPA in MATLAB, comparing 1000 simulated positioning nodes of CTFPA and the Caffery positioning algorithm (CPA) for a 95 m long tunnel. The positioning error field of the tunnel was established, and the influence of the spatial variation on the positioning accuracy of CPA and CTFPA was analysed. The simulation results show that, compared with CPA, the positioning accuracy of CTFPA is clearly improved, and the accuracy of each axis can reach more than 5 mm. The accuracy of the X-axis is higher than that of the Y-and Z-axes. In section X-Y of the tunnel, the root mean square error (RMSE) contours of CTFPA are clear and orderly, and with an increase in the measuring distance, RMSE increases linearly. In section X-Z, the RMSE contours are concentric circles, and the variation ratio is nonlinear.

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The long noncoding RNA (lncRNA) LINC00152, also known as CYTOR, displays aberrant expression in various cancers. However, its clinical value and functional mechanisms in breast cancer remain insufficiently understood. Our study found that LINC00152 is significantly upregulated in breast cancer, and that it acts as an indicator of poor survival prognosis. Further studies revealed that LINC00152 knockdown suppresses cell proliferation and tumorigenicity in vitro and in vivo. Mechanistic analyses demonstrated that LINC00152 directly binds to KLF5 protein and increases KLF5 stability. Moreover, LINC00152 is also a KLF5-responsive lncRNA, and KLF5 activates LINC00152 transcription by directly binding to its promoter. Our study suggests that LINC00152 promotes tumor progression by interacting with KLF5. LINC00152 may be a valuable prognostic predictor for breast cancer, and the positive feedback loop of LINC00152-KLF5 could be a therapeutic target in pharmacological strategies.