m6A-methylated KCTD21-AS1 regulates macrophage phagocytosis through CD47 and cell autophagy through TIPR.

Blocking immune checkpoint CD47/SIRPα is a useful strategy to engineer macrophages for cancer immunotherapy. However, the roles of CD47-related noncoding RNA in regulating macrophage phagocytosis for lung cancer therapy remain unclear. This study aims to investigate the effects of long noncoding RNA (lncRNA) on the phagocytosis of macrophage via CD47 and the proliferation of non-small cell lung cancer (NSCLC) via TIPRL. Our results demonstrate that lncRNA KCTD21-AS1 increases in NSCLC tissues and is associated with poor survival of patients. KCTD21-AS1 and its m6A modification by Mettl14 promote NSCLC cell proliferation. miR-519d-5p gain suppresses the proliferation and metastasis of NSCLC cells by regulating CD47 and TIPRL. Through ceRNA with miR-519d-5p, KCTD21-AS1 regulates the expression of CD47 and TIPRL, which further regulates macrophage phagocytosis and cancer cell autophagy. Low miR-519d-5p in patients with NSCLC corresponds with poor survival. High TIPRL or CD47 levels in patients with NSCLC corresponds with poor survival. In conclusion, we demonstrate that KCTD21-AS1 and its m6A modification promote NSCLC cell proliferation, whereas miR-519d-5p inhibits this process by regulating CD47 and TIPRL expression, which further affects macrophage phagocytosis and cell autophagy. This study provides a strategy through miR-519-5p gain or KCTD21-AS1 depletion for NSCLC therapy by regulating CD47 and TIPRL.

Environmental Applications of 3D g-C3N4-Based Hydrogel with Synergistic Effect of Adsorption and Photodegradation.

In this paper, g-C3N4-based hydrogel with a 3D network structure was synthesized via a simple and cheap reaction, using hydroxyethyl cellulose (HEC) and graphitic carbon nitride (g-C3N4) as the main materials. Electron microscope images revealed that the microstructure of g-C3N4-HEC hydrogel was rough and porous. The luxuriant scaly textures of this hydrogel were due to the uniform distribution of g-C3N4 nanoparticles. It was found that this hydrogel showed great removal ability of bisphenol A (BPA) through a synergistic effect of adsorption and photodegradation. The adsorption capacity and degradation efficiency of g-C3N4-HEC hydrogel (3%) for BPA were 8.66 mg/g and 78% under the conditions of C0 = 9.94 mg/L and pH = 7.0, which were much higher than those for the original g-C3N4 and HEC hydrogel. In addition, g-C3N4-HEC hydrogel (3%) exhibited excellent removal efficiency (98%) of BPA (C0 = 9.94 mg/L) in a dynamic adsorption and photodegradation system. Meanwhile, the mechanism of removal was investigated in depth. The superior batch and continuous removal capability of this g-C3N4-based hydrogel make it promising for environmental applications.

WFDC21P promotes triple-negative breast cancer proliferation and migration through WFDC21P/miR-628/SMAD3 axis.

Long non-coding RNAs (lncRNAs) modulate cell proliferation, cycle, and apoptosis. However, the role of lncRNA-WFDC21P in the tumorigenesis of triple-negative breast cancer (TNBC) remains unclear. Results of this study demonstrated that WFDC21P levels significantly increased in TNBC, which was associated with the poor survival of patients. WFDC21P overexpression significantly promoted TNBC cell proliferation and metastasis. WFDC21P interacted with miR-628-5p, which further suppressed cell proliferation and metastasis by negatively regulating Smad3-related gene expression. Recovery of miR-628-5p weakened the roles of WFDC21P in promoting the growth and metastasis of TNBC cells. Moreover,N6-methyladenosine (m6A) modification upregulated WFDC21P expression in the TNBC cells. WFDC21P and its m6A levels were increased after methyltransferase like 3 (METTL3) overexpression but reduced after METTL3 silencing. The proliferation and metastasis of TNBC cells were promoted by METTL3 overexpression but suppressed by METTL3 silencing. This study demonstrated the vital roles of WFDC21P and its m6A in regulating the proliferation and metastasis of TNBC cells via the WFDC21P/miR-628/SMAD3 axis.

Oncogenic TRIB2 interacts with and regulates PKM2 to promote aerobic glycolysis and lung cancer cell procession.

PKM2 is an important regulator of the aerobic glycolysis that plays a vital role in cancer cell metabolic reprogramming. In general, Trib2 is considered as a "pseudokinase", contributing to different kinds of cancer. However, the detailed roles of TRIB2 in regulating cancer metabolism by PKM2 remain unclear. This study demonstrated that TRIB2, not a "pseudokinase", has the kinase activity to directly phosphorylate PKM2 at serine 37 in cancer cells. The elevated pSer37-PKM2 would subsequently promote the PKM2 dimers to enter into nucleus and increase the expression of LDHA, GLUT1, and PTBP1. The aerobic glycolysis is then elevated to promote cancer cell proliferation and migration in TRIB2- or PKM2-overexpressed cultures. The glucose uptake and lactate production increased, but the ATP content decreased in TRIB2- or PKM2-treated cultures. Experiments of TRIB2-/- mice further supported that TRIB2 could regulate aerobic glycolysis by PKM2. Thus, these results reveal the new kinase activity of TRIB2 and its mechanism in cancer metabolism may be related to regulating PKM2 to promote lung cancer cell proliferation in vitro and in vivo, suggesting promising therapeutic targets for cancer therapy by controlling cancer metabolism.

Highly efficient catalytic ozonation for ammonium in water upon γ-Al2O3@Fe/Mg with acidic-basic sites and oxygen vacancies.

Catalytic ozonation has prospects in the advanced treatment of nitrogen removal, and solid base MgO can efficiently catalyze the ozonation of ammonium nitrogen. However, it is necessary to improve the problem of easy loss, difficult recovery, and low percentage of gaseous products. Here, MgO, amorphous Fe2O3, and γ-Al2O3 were selected as doping components and supports, respectively, to prepare γ-Al2O3@Fe/Mg composite catalysts with abundant acidic-basic sites and oxygen vacancies. The results show that γ-Al2O3@Fe/Mg5 can efficiently catalyze the ozonation of ammonium nitrogen (98.73%) with 67.82% gaseous product selectivity under the conditions of initial pH = 7, catalyst dosage of 112.88 g/L, and ozone dosage of 2.4 mg/min. The doping of Fe2O3 and MgO with a weaker lattice oxygen binding energy improves the gaseous product selectivity. The mechanism of ammonium nitrogen removal for γ-Al2O3@Fe/Mg5 is revealed, especially the intrinsic contribution of acidic-basic sites and oxygen vacancies. The pH and active sites play different roles in ozone decomposition for NH4+ removal. Surface hydroxyl protonation on basic sites and oxygen vacancies and electron transfer on acidic sites are responsible for ozone decomposition to hydroxyl radicals. Moreover, γ-Al2O3@Fe/Mg5 exhibits good stability, few leaching ions, and can be settled in water for easy recovery. This study suggests that γ-Al2O3@Fe/Mg5 is a good candidate for the catalytic ozonation of ammonium nitrogen.

TRIB2 regulates the expression of miR­33a­5p through the ERK/c­Fos pathway to affect the imatinib resistance of chronic myeloid leukemia cells.

Chronic myeloid leukemia (CML) is a hematological disease, and imatinib (IM) resistance represents a major problem for its clinical treatment. In the present study, the role of tribbles pseudokinase 2 (TRIB2) in IM resistance of CML and the possible mechanism were investigated. It was found that TRIB2 was highly expressed in IM­resistant patients with CML through the Oncomine database and this conclusion was confirmed using reverse transcription­quantitative PCR and western blot experiments. Knockdown of TRIB2 was found to increase the drug sensitivity of KG cells to IM using Cell­Counting Kit­8 (CCK­8) assays, and the low­expression TRIB2 mice were further found to be more sensitive to the IM and have a higher survival rate in leukemia model mice. Moreover, using western blot and luciferase experiments, it was found that TRIB2 could regulate c­Fos through the ERK signaling pathway, and c­Fos suppressed the transcriptional activity and the expression of miR­33a­5p. Further investigation identified that the binding site for c­Fos to function on miR­33a­5p was the ­958­965 region. Finally, CCK­8 assays and western blot experiments demonstrated that miR­33a­5p could inhibit the proliferation of KG cells and reduce IM resistance by suppressing the expression of HMGA2. In conclusion, it was demonstrated that TRIB2 regulates miR­33a­5p to reverse IM resistance in CML, which may help identify novel targets and therapeutic strategies for the clinical treatment of IM resistance.

RFWD2 Knockdown as a Blocker to Reverse the Oncogenic Role of TRIB2 in Lung Adenocarcinoma.

RFWD2, an E3 ubiquitin ligase, is overexpressed in numerous human cancers, including leukemia, lung cancer, breast cancer, renal cell carcinoma, and colorectal cancer. The roles of RFWD2 in cancer are related to the targeting of its substrates for ubiquitination and degradation. This study aimed to investigate the role of TRIB2 in relation to the regulation of protein degradation through RFWD2. inBio Discover™ results demonstrated that TRIB2 can perform its functions by interacting with RFWD2 or other factors. TRIB2 can interact with and regulate RFWD2, which further attends the proteasome-mediated degradation of the RFWD2 substrate p-IκB-α. TRIB2 colocalizes with RFWD2-related IκB-α to form a ternary complex and further affects the IκB-α degradation by regulating its phosphorylation. Specific domain analysis showed that TRIB2 may bind to RFWD2 via its C-terminus, whereas it binds to IκB via its pseudokinase domain. TRIB2 acts as an oncogene and promotes cancer cell proliferation and migration, whereas RFWD2 knockdown reversed the role of TRIB2 in promoting cancer cell growth and colony formation in vitro and in vivo. In summary, this study reveals that TRIB2 promotes the progression of cancer by affecting the proteasome-mediated degradation of proteins through the interaction with RFWD2.

Profiling of co-metabolic degradation of tetracycline by the bio-cathode in microbial fuel cells.

In this paper, a system of tetracycline (TEC) degradation by the bio-cathode in a microbial fuel cell (MFC) was constructed. Overall, the co-metabolic degradation performance of TEC was studied through single factor experiments and the ecological risk was evaluated using the E. coli growth inhibition rate and resistance genes. High throughput sequencing (HTS) was utilized to profile the biofilm community structure of the bio-cathode. Results showed that the degradation rate of TEC reached greater than 90% under optimal conditions, which was 10 mg L-1 initial TEC concentration, 0.2-0.7 g L-1 sodium acetate concentration and 12-18 L h-1 aeration. Furthermore, compared with the aerobic biodegradation of TEC, the degradation efficiency of the MFC bio-cathode for TEC was significantly increased by 50% and the eco-toxicity of TEC after 36 hour degradation was reduced by 60.9%, and TEC ARGs in effluent were cut down. HTS results showed that electrochemically active bacteria Acetobacter and TEC-resistant degradation bacteria Hyphomicrobium, Clostridium and Rhodopseudomonas were the main dominant bacteria in the cathode biofilm. Besides, based on 5 intermediates, degradation pathways involving deamidation, denitro dimethylation, dedimethylation and dehydroxylation of TEC were proposed. The degradation of TEC on the bio-cathode was mainly caused by microbial co-metabolism action. This study would enrich the study of MFC bio-cathodic degradation of antibiotics in water.

Bioaugmentation of Moving Bed Biofilm Reactor (MBBR) with Achromobacter JL9 for enhanced sulfamethoxazole (SMX) degradation in aquaculture wastewater.

This study investigated whether bioaugmentation improves sulfamethoxazole (SMX) degradation and nitrogen removal in the Moving Bed Biofilm Reactor (MBBR) system. The effects of the C/N ratio on SMX degradation and nitrogen removal were also evaluated. Using MBBR system operation experiments, the bioaugmented reactor was found to perform more effectively than the non-bioaugmentation reactor, with the highest SMX, nitrate-N, and ammonia-N removal efficiencies of 80.49, 94.70, and 96.09%, respectively. The changes in the sulfonamide resistance genes and bacterial communities were detected at various operating conditions. The results indicate that the diversity of the bacterial communities and the abundance of resistance genes were markedly influenced by bioaugmentation and the C/N ratio, with Achromobacter among the dominant genera in the MBBR system. The bio-toxicity of samples, calculated as the inhibition percentage (IP) toward Escherichia coli, was found to decrease to non-toxic ranges after treatment.