METTL3-dependent m6A modification mediates bladder remodeling after partial bladder outlet obstruction through CCN2 activation.

Aims: N6-methyladenosine (m6A) modification is a critical posttranscriptional event in gene regulation. Thus, identifying methyltransferase, demethylase, or m6A binding protein-mediated m6A modifications in cancer or noncancer transcriptomes has become a promising novel strategy for disease therapy development. However, novel insights into m6A modification in partial bladder outlet obstruction (pBOO) and detailed information about the drivers of bladder remodeling remain to be elucidated.

Roles of DNA damage repair and precise targeted therapy in renal cancer (Review).

The primary subtypes of renal cell carcinoma (RCC) include clear cell, papillary and chromophobe RCC. RCC occurs often due to loss of von Hippel‑Lindau (VHL) and accumulation of lipids and glycogen, and RCC cells may exhibit sensitivity to the disruption of normal metabolism or homologous recombination gene defect. Although the application of molecular‑targeted drugs (tyrosine kinase inhibitors) and immune checkpoint inhibitors has been recommended for the treatment of advanced RCC, more targets of DNA damage repair (DDR) signaling pathway involved in the synthetic lethal effect have been investigated.

LncRNA LINC00944 Promotes Tumorigenesis but Suppresses Akt Phosphorylation in Renal Cell Carcinoma.

Long non-coding RNA (lncRNA) is a kind of RNA that possesses longer than 200 nucleotides and lacks protein coding function. It was recognized as a junk sequence for a long time. Recent studies have found that lncRNAs are actively functioning in almost every aspect of cell biology and involved in a variety of biological functions.

Downregulation of CacyBP by CRISPR/dCas9-KRAB Prevents Bladder Cancer Progression.

Bladder cancer (BCa) is a leading cause of cancer-related death in the world. CacyBP is initially described as a binding partner of calcyclin and has been shown to be involved in a wide range of cellular processes, including cell differentiation, proliferation, protein ubiquitination, cytoskeletal dynamics and tumorigenesis. In the present study, we found that CacyBP expression was significantly upregulated in BCa tissues compared with adjacent normal tissues.

The tumour microenvironment and metabolism in renal cell carcinoma targeted or immune therapy.

Renal cell carcinoma (RCC) is one of the most common tumours of the urinary system, and is insidious and not susceptible to chemoradiotherapy. As the most common subtype of RCC (70-80% of cases), clear cell renal cell carcinoma (ccRCC) is characterized by the loss of von Hippel-Lindau and the accumulation of robust lipid and glycogen. For advanced RCC, molecular-targeted drugs, tyrosine kinase inhibitors (TKIs) and the immune checkpoint inhibitors (ICIs) have been increasingly recommended and investigated.

Sputtered ZnO-SiO2 nanocomposite light-emitting diodes with flat-top nanosecond laser treatment.

Sputtered ZnO-SiO2 nanocomposite light-emitting diodes (LEDs) were treated using a flat-top nanosecond laser (FTNL) under room temperature. The intensity of the 376 nm electroluminescence (EL) emission of ZnO-SiO2 nanocomposite LEDs at a current of 9 mA with FTNL treatment was approximately 1.4 times greater than LEDs without FTNL treatment.

Electroluminescence of ZnO nanocrystal in sputtered ZnO-SiO2 nanocomposite light-emitting devices.

We have demonstrated the electroluminescence (EL) of Ga:ZnO/i-ZnO-SiO2 nanocomposite/p-GaN n-i-p heterostructure light-emitting devices (LEDs). ZnO nano-clusters with sizes distributing from 2 to 7nm were found inside the co-sputtered i-ZnO-SiO2 nanocomposite layer under the observation of high-resolution transparent electron microscope. A clear UV EL at 376 nm from i-ZnO-SiO2 nanocomposite in these p-i-n heterostructure LEDs was observed under the forward current of 9 mA.