Photochromism, Thermochromism, and Electrochromism in Solid-State Host-Guest Inclusion Complexes of ß-Cyclodextrin with Dialkylcarboxyl-Substituted Viologens.

Multi-stimuli-responsive chromic materials have immense potential for utilization. Herein, two supramolecular inclusion complexes were prepared by self-assembly of ß-cyclodextrin (ß-CD) with dialkylcarboxyl-substituted viologens, N,N'-di(3-carboxy-propyl)-4,4'-bipyridinium dichloride (CPV·Cl2) and N,N'-di(6-carboxy-hexyl)-4,4'-bipyridinium dibromide (CHV·Br2). The self-assembled inclusion complexes CPV2+@ß-CD and CHV2+@ß-CD2 in the solid-state exhibited naked-eye photochromism, thermochromism, and electrochromism in response to multiple external stimuli including light, temperature, and electric field, respectively. Solid-state UV-vis diffuse reflectance and electron spin resonance (ESR) spectroscopy revealed that the observed photochromism, thermochromism and electrochromism are attributed to the formation of viologen free radicals induced by electron transfer under external stimuli. The excellent stimuli-response chromic properties of the title inclusion complexes support their practical utility in visual display, multiple anticounterfeiting, and multilevel information encryption.

RNF168 facilitates proliferation and invasion of esophageal carcinoma, possibly via stabilizing STAT1.

Oesophageal cancer ranks as one of the most common malignancy in China and worldwide. Although genome-wide association studies and molecular biology studies aim to elucidate the driver molecules in oesophageal cancer progression, the detailed mechanisms remain to be identified. Interestingly, RNF168 (RING finger protein 168) shows a high frequency of gene amplification in oesophageal cancer from TCGA database. Here, we report an important function for RNF168 protein in supporting oesophageal cancer growth and invasion by stabilizing STAT1 protein. RNF168 gene is amplified in oesophageal cancer samples, which tends to correlate with poor prognosis. Depletion RNF168 causes decreased cell proliferation and invasion in oesophageal cancer cells. Through unbiased RNA sequencing in RNF168 depleted oesophageal cancer cell, we identifies JAK-STAT pathway is dramatically decreased. Depletion RNF168 reduced JAK-STAT target genes, such as IRF1, IRF9 and IFITM1. Immuno-precipitation reveals that RNF168 associates with STAT1 in the nucleus, stabilizing STAT1 protein and inhibiting its poly-ubiquitination and degradation. Our study provides a novel mechanism that RNF168 promoting JAK-STAT signalling in supporting oesophageal cancer progression. It could be a promising strategy to target RNF168 for oesophageal cancer treatment.