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Regenerative electroless etching (ReEtching), described herein for the first time, is a method of producing nanostructured semiconductors in which an oxidant (Ox ) is used as a catalytic agent to facilitate the reaction between a semiconductor and a second oxidant (Ox ) that would be unreactive in the primary reaction. Ox is used to regenerate Ox , which is capable of initiating etching by injecting holes into the semiconductor valence band. Therefore, the extent of reaction is controlled by the amount of Ox added, and the rate of reaction is controlled by the injection rate of Ox . This general strategy is demonstrated specifically for the production of highly luminescent, nanocrystalline porous Si from the reaction of V O in HF(aq) as Ox and H O (aq) as Ox with Si powder and wafers.

Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) is regarded as an oncogene in multiple cancers. Previous studies have shown that NEAT1 is involved in the proliferation and tumorigenesis of glioma cells, while miR-185-5p functions as a tumor suppressor in glioma. However, the underlying molecular mechanism of NEAT1 in glioma, especially in association with miR-185-5p, has not been studied. In this study, we first demonstrated that NEAT1 expression was upregulated, and miR-185-5p downregulated in glioma tissues and cells. More important, NEAT1 expression was negatively correlated with miR-185-5p expression in glioma tissues. In vitro and in vivo experiments verified that NEAT1 was a competing endogenous RNA for miR-185-5p for promoting DNA methyltransferase 1 (DNMT1) expression and activated mammalian target of rapamycin (mTOR) signaling, thus inhibiting apoptosis, and promoting glioma migration, proliferation, and epithelial-mesenchymal transition process. Furthermore, NEAT1 knockdown suppressed tumor growth and reduced the expression of proliferation antigen Ki-67, DNMT1, and mTOR, but upregulated the expression of miR-185-5p in vivo. Finally, with mTOR inhibitor rapamycin, we confirmed that NEAT1 promoted glioma activity through mTOR signaling both in vitro and in vivo. In conclusion, these results suggest that NEAT1 promotes glioma tumorigenesis via miR-185-5p/DNMT1/mTOR signaling, which may provide a new target for the diagnosis and therapy of glioma.