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Colon cancer is the fourth leading cause of cancer-related death, and exhibited clinical differences among patients of different ages, including malignancy, metastasis, and mortality rate. Few studies, however, focus on the communications between aging and colon cancer. Here we identified age-dependent differentially expressed genes (DEGs) in colon cancer using TCGA transcriptome data. Through analyzing multi-omics high throughput data, including ATAC-Seq, DNaseI-Seq and ChIP-Seq, we obtained six age-dependent transcription factors in colon cancer, and their age-dependent targets, significantly affecting patients’ overall survivals. Transcription factor ETS1 potentially functioned in both aging process and colon cancer progression through regulating its targets, RGL2 and SLC2A3. In addition, comparing with its relative lower expression levels in elderly patients, higher levels of RGL2 were detected in young patients, and significantly associated with larger tumor size, higher metastasis, and invasions of colon cancer, consistent with the clinical traits that young patients’ colon cancer exhibited late stages with more aggressiveness. Thus, these elements may serve as keys linking aging and colon cancer, and providing new insights and basis for mechanism researches, as well as diagnosis and therapies of colon cancer, especially in young patients.

Various electrochemical separation methods have been investigated for the recovery of lithium to satisfy the global demand for lithium. However, most of them are still greatly limited by high energy consumption and deficient selectivity. To overcome these issues, in this study, an electrically switched ion exchange (ESIX) system for efficient and selective LiCl separation from brine lakes was developed based on a strategy of self-electrical-energy recuperation, in which the electric energy generated in the process of LiCl uptake was proposed to compensate the energy consumed for the desorption of ions as well as the regeneration of electrodes. λ-MnO2 film coated electrode and BiOCl@PPy film coated electrode were fabricated to capture Li+ and Cl- ions in the brine lake, respectively. In the ion uptake process, the inherent potential difference between the two electrodes was balanced due to the embeddedness of Li+ and Cl- ions, which simultaneously triggered the generation of electric energy. This generated electric energy was automatically stored and provided for the desorption of the Li+ and Cl- ions from the electrodes in the ion releasing process. As a result, this ESIX system featured with extremely low energy consumption (1.007 Wh for separating per mole of LiCl) and excellent selectivity with a LiCl recovery capacity of 10.88 mg/g. It is expected that such an ESIX system with self-electrical-energy recuperation could be a promising alternative to those current electrochemical techniques for the recovery of LiCl from brine lakes.

SummaryPTPN12 is an important tumor suppressor that plays critical roles in various physiological processes. However, the molecular basis underlying the substrate specificity of PTPN12 remains uncertain. Here, enzymological and crystallographic studies have enabled us to identify two distinct structural features that are crucial determinants of PTPN12 substrate specificity: the pY+1 site binding pocket and specific basic charged residues along its surface loops. Key structurally plastic regions and specific residues in PTPN12 enabled recognition of different HER2 phosphorylation sites and regulated specific PTPN12 functions. In addition, the structure of PTPN12 revealed a CDK2 phosphorylation site in a specific PTPN12 loop. Taken together, our results not only provide the working mechanisms of PTPN12 for desphosphorylation of its substrates but will also help in designing specific inhibitors of PTPN12.

Sunlight exposure is known to affect mood, learning, and cognition. However, the molecular and cellular mechanisms remain elusive. Here, we show that moderate UV exposure elevated blood urocanic acid (UCA), which then crossed the blood-brain barrier. Single-cell mass spectrometry and isotopic labeling revealed a novel intra-neuronal metabolic pathway converting UCA to glutamate (GLU) after UV exposure. This UV-triggered GLU synthesis promoted its packaging into synaptic vesicles and its release at glutamatergic terminals in the motor cortex and hippocampus. Related behaviors, like rotarod learning and object recognition memory, were enhanced after UV exposure. All UV-induced metabolic, electrophysiological, and behavioral effects could be reproduced by the intravenous injection of UCA and diminished by the application of inhibitor or short hairpin RNA (shRNA) against urocanase, an enzyme critical for the conversion of UCA to GLU. These findings reveal a new GLU biosynthetic pathway, which could contribute to some of the sunlight-induced neurobehavioral changes.