Identification of Potential Diagnostic and Prognostic Biomarkers for Gastric Cancer Based on Bioinformatic Analysis.

Gastric cancer (GC) ranks third for cancer-related fatalities worldwide. It is still unclear what causes GC to progress. Using integrated bioinformatics analysis, COL5A2 has been proved to be related to GC development, which may identify the likely pathogenic mechanism. Data from GC patients were gathered using The Cancer Gene Atlas (TCGA) and the gene expression omnibus (GEO). The level of COL5A2 expression was compared between paired GC and normal tissues. The differentially expressed genes (DEGs) in GC patients with high and low COL5A2 expression were identified using functional enrichment analysis to identify the signature pathways linked to the DEGs. The clinical pathologic traits connected to overall survival (OS) of GC patients were examined utilizing Cox regression and the Kaplan-Meier method. To assess the prognostic significance of COL5A2, receiver operating characteristic (ROC) curves was drawn. How the immune system infiltrate both normal gastric and GC tumor tissues was investigated. Using the human protein atlas (HPA) database, regression, and the Kaplan-Meier method, immunohistochemical analysis of DEG COL5A2 expression in GC tissues was carried out. The correlation between COL5A2 expression and the GC grouping was found to be highly significant. Functional annotations revealed that COL5A2 participates in extracellular matrix structure, collagen metabolism, and other biological processes (BPs). High COL5A2 expression was associated with poor prognostic and clinical features, such as clinical T, N, and M stages. ROC curves exhibited that COL5A2 might predict the occurrence of gastric cancer. The infiltration degree of 21 immune cell subsets, including activated dendritic cells (aDCs), CD8+ T cells, and cytotoxic cells, was found to be dramatically relevant to COL5A2. Immunohistochemical analysis indicated that the expression of COL5A2 in tumor tissues is higher than that in normal tissues. The COL5A2 gene may offer fresh perspectives on the pathogenic mechanism underlying GC, as well as potential biomarkers for estimating GC patient prognosis. As a result, COL5A2 may be a useful biomarker for predicting patient survival.

Preliminary report on the short-term efficacy and safety of SAPO-S1 therapy for locally advanced gastric cancer with a deep learning perspective.

The neoadjuvant therapeutic effects of various chemotherapeutic drugs on gastric cancer have reached the corresponding plateau. Whether the combination of sindilizumab and albumin-bound paclitaxel+oxaliplatin+S-1 chemotherapy (SAPO-S1 therapy) regimen can bring better efficacy and observe the incidence of adverse reactions in the neoadjuvant treatment of Gastric Cancer (GC) may be the direction of our research. This study aimed to evaluate the efficacy of S1 chemotherapy regimen combined with multiple chemotherapy drugs sindilizumab (PD-1 inhibitor), albumin-bound paclitaxel and oxaliplatin) for neoadjuvant therapy in locally advanced Gastric Cancer (LA-GC). The patients were given 4 cycles of sindilizumab combined with albumin paclitaxel+oxaliplatin+S-1 chemotherapy (SAPO-S1) before surgery. The R0 resection rate, surgical complications, pathologic complete response, complete pathologic response (pCR) the main pathological response rates (residual tumor cells≤10%, major pathological response) were observed. MPR and postoperative pathological tumor regression grade (TRG), using the response evaluation criteria in solid tumors (RECIST1.1) to evaluate the efficacy of new adjuvant therapy and record the short-term adverse events (adverse event, AE) of patients after medication to evaluate safety. The overall response rate (ORR) was achieved to 53.3% and disease control rate (DCR) was achieved in 28 patients (93.3%), and the descending phase was achieved in 17 patients (56.7%). The tumor resolution grades of TRG 0, TRG 1, TRG 2 and TRG 3 were 16.7%, 13.3%, 43.3% and 16.7%, respectively. The pCR rate was 16.7%, the MPR rate was 30.0%, and the R0 resection rate was 90.0%. In addition, SAPO-S1 therapy has fewer side effects. Overall, SAPO-S1 therapy has a good therapeutic effect and safety in LA-GC.

Structurally Regulated Carbazole-Pyridine Derivatives Based on Space-Crowded Theory for Efficient Narrowband Ultraviolet Nondoped Organic Light-Emitting Diodes from the High-Lying Reverse Intersystem Crossing Process.

Achieving ultraviolet and narrowband emission simultaneously in nondoped organic light-emitting diodes (OLEDs) remains a tremendous challenge. Here, a "space-crowded donor-acceptor-donor" molecular design strategy is proposed for developing ultraviolet pure organic fluorophores by the nearby substituted positions at the phenyl linker between carbazole and pyridine units. Benefitting from the large steric hindrance effect, multiple intramolecular interactions, and low-frequency vibronic coupling dominated excited state property, all the emitters exhibit excellent fluorescence efficiencies at the solid state as well as the narrow full width at half maximums (FWHMs). Moreover, the effect of different substitution positions of pyridine on the structure-property relationship is also revealed. Consequently, the nondoped OLEDs exhibit an electroluminescence emission peak of 397 nm with FWHMs of 17 and 22 nm. Due to the high-lying reverse intersystem crossing process, external quantum and exciton utilization efficiencies of 3.6 and 54.55%, respectively, have been achieved based on the emitter with para-linkage. These findings may pave an avenue for the development of high-performance narrowband ultraviolet materials and OLEDs.

COPS3 Promotes Proliferation, Invasion, and EMT of Colorectal Cancer Cells by MEK/ERK Pathway.

Colorectal cancer (CRC) is one of the most aggressive cancers with poor prognosis and high mortality. The study of the pathogenesis of CRC is a top priority in providing effective diagnostic and prognostic strategies for CRC. COPS3 protein is a subunit of the COP9 signaling body (CSN), which is closely associated with the development of multiple types of tumors. However, there are few studies on the role of COPS3 in colon adenocarcinoma (COAD). This study investigated the effects of COPS3 on proliferation, motility, and EMT of colorectal cancer cells and related mechanisms. COPS3 was highly expressed in COAD. The depletion of COPS3 suppressed the viability and stimulated the apoptosis of COAD cells. Depletion of COPS3 suppressed the motility and EMT process of COAD cells. Mechanically, we found that COPS3 could mediate MEK/ERK pathway and therefore affected the process of COAD cells. We thought that COPS3 could serve as a promising COAD target.