EYA4 Promotes Cell Proliferation Through Downregulation of p27Kip1 in Glioma

Background/Aims: Accumulating evidence suggests that Eyes Absent Homologue 4 (EYA4) plays an important role in tumorigenesis and progression of various cancers. However, the role of EYA4 in glioma development is still unclear. Methods: The expression of EYA4 was examined in glioma tissues by immunohistochemistry. Cell viability and apoptosis were analyzed by CCK-8, BrdU assay, and flow cytometry. Results: We found that EYA4 was upregulated in glioma, and its expression was positively correlated with advanced tumor stage. Moreover, higher expression of EYA4 predicted a worse overall survival in patients with glioma. Forced overexpression of EYA4 enhanced glioma cell proliferation, and EYA4 suppressed the expression of p27Kip1 directly in these cells. Furthermore, Six1 was required for EYA4 to suppress the expression of p27Kip1 in glioma. Conclusion: Together, we demonstrate that EYA4 promotes cell proliferation by directly suppressing the expression of p27Kip1 in glioma

SNHG6 Promotes Tumor Growth via Repression of P21 in Colorectal Cancer

Background/Aims: SNHG6 (Small Nucleolar RNA Host Gene 6) is a novel non-coding RNA (ncRNA) and its cellular function is largely unknown. Methods: Cell Counting Kit-8 (CCK-8) cell growth assay, colony formation and flow cytometry were used to determine colorectal cancer cell proliferation, cell cycle progression and apoptosis in vitro. The xenograft tumor formation assay in nude mice was established to evaluate tumor growth in vivo. RNA immunopreciptation (RIP) analysis was performed to examine whether SNHG6 could bind to EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit), and chromatin immunoprecipitation (ChIP) assay was conducted to examine whether SNHG6 could repress p21 transcription by recruiting EZH2 to the p21 promoter. Results: Here we found that SNHG6 was upregulated and its expression levels were positively correlated with advanced tumor stage in colorectal cancer. Survival analysis suggested that higher expression of SNHG6 predicted poor prognosis in patients with colorectal cancer. Functional studies indicated that SNHG6 could promote cell proliferation via a direct suppression of p21 expression in colorectal cancer cells. Moreover, SNHG6 repressed p21 transcription through recruiting EZH2 to the p21 promoter in colorectal cancer cells. Conclusion: Taken together, our study demonstrates that SNHG6 promotes tumor growth via repression of p21 in colorectal cancer, which may provide a promising target for novel anticancer therapeutics

Inconsistency of QED in the Presence of Dirac Monopoles

A precise formulation of $U(1)$ local gauge invariance in QED is presented, which clearly shows that the gauge coupling associated with the unphysical longitudinal photon field is non-observable and actually has an arbitrary value. We then re-examine the Dirac quantization condition and find that its derivation involves solely the unphysical longitudinal coupling. Hence an inconsistency inevitably arises in the presence of Dirac monopoles and this can be considered as a theoretical evidence against their existence. An alternative, independent proof of this conclusion is also presented.Comment: Extended and combined version, refinements added; 20 LaTex pages, Published in Z. Phys. C65, pp.175-18

An MDA-Based System for Ontology Engineering

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