Tumor-suppressor activity of RRIG1 in breast cancer

<p>Abstract</p> <p>Background</p> <p>Retinoid receptor-induced gene-1 (RRIG1) is a novel gene that has been lost in several types of human cancers. The aim of this study was to determine whether RRIG1 plays a role in breast cancer, such as in the suppression of breast cancer cell growth and invasion.</p> <p>Methods</p> <p>Immunohistochemistry was used to detect RRIG1 expression in breast tissue specimens. Gene transfection was used to restore or knock down RRIG1 expression in breast cancer cell lines for analysis of cell viability, colony formation, and migration/invasion potential. Reverse-transcription polymerase chain reaction and western blot assays were used to detect the changes in gene expression. The RhoA activation assay was used to assess RRIG1-induced inhibition of RhoA activity.</p> <p>Results</p> <p>The immunohistochemical data showed that <it>RRIG1 </it>expression was reduced in breast cancer tissues compared with normal and atypical hyperplastic breast tissues. <it>RRIG1 </it>expression was inversely correlated with lymph node metastasis of breast cancer but was not associated with the status of hormone receptors, such as estrogen receptor, progesterone receptor, or HER2. Furthermore, restoration of <it>RRIG1 </it>expression inhibited proliferation, colony formation, migration, and invasion of breast cancer cells. Expression of RRIG1 also reduced phosphorylated Erk1/2 and Akt levels; c-Jun, MMP9, and Akt expressions; and RhoA activity. In contrast, knockdown of RRIG1 expression promoted breast cancer cell proliferation, colony formation, migration, and invasion potential.</p> <p>Conclusion</p> <p>The data from the current study indicated that <it>RRIG1 </it>expression was reduced or lost in breast cancer and that restoration of RRIG1 expression suppressed breast cancer cell growth and invasion capacity. Future studies will determine the underlying molecular mechanisms and define RRIG1 as a tumor-suppressor gene in breast cancer.</p

Damping signatures at JUNO, a medium-baseline reactor neutrino oscillation experiment

Abstract We study damping signatures at the Jiangmen Underground Neutrino Observatory (JUNO), a medium-baseline reactor neutrino oscillation experiment. These damping signatures are motivated by various new physics models, including quantum decoherence, nu(3) decay, neutrino absorption, and wave packet decoherence. The phenomenological effects of these models can be characterized by exponential damping factors at the probability level. We assess how well JUNO can constrain these damping parameters and how to disentangle these different damping signatures at JUNO. Compared to current experimental limits, JUNO can significantly improve the limits on tau(3)/m(3) in the nu(3) decay model, the width of the neutrino wave packet sigma(x), and the intrinsic relative dispersion of neutrino momentum sigma(rel)

JUNO sensitivity to the annihilation of MeV dark matter in the galactic halo

International audienceWe discuss JUNO sensitivity to the annihilation of MeV dark matter in the galactic halo via detecting inverse beta decay reactions of electron anti-neutrinos resulting from the annihilation. We study possible backgrounds to the signature, including the reactor neutrinos, diffuse supernova neutrino background, charged- and neutral-current interactions of atmospheric neutrinos, backgrounds from muon-induced fast neutrons and cosmogenic isotopes. A fiducial volume cut, as well as the pulse shape discrimination and the muon veto are applied to suppress the above backgrounds. It is shown that JUNO sensitivity to the thermally averaged dark matter annihilation rate in 10 years of exposure would be significantly better than the present-day best limit set by Super-Kamiokande and would be comparable to that expected by Hyper-Kamiokande