Tip60-mediated H2A.Z acetylation promotes neuronal fate specification and bivalent gene activation.

Cell lineage specification is accomplished by a concerted action of chromatin remodeling and tissue-specific transcription factors. However, the mechanisms that induce and maintain appropriate lineage-specific gene expression remain elusive. Here, we used an unbiased proteomics approach to characterize chromatin regulators that mediate the induction of neuronal cell fate. We found that Tip60 acetyltransferase is essential to establish neuronal cell identity partly via acetylation of the histone variant H2A.Z. Despite its tight correlation with gene expression and active chromatin, loss of H2A.Z acetylation had little effect on chromatin accessibility or transcription. Instead, loss of Tip60 and acetyl-H2A.Z interfered with H3K4me3 deposition and activation of a unique subset of silent, lineage-restricted genes characterized by a bivalent chromatin configuration at their promoters. Altogether, our results illuminate the mechanisms underlying bivalent chromatin activation and reveal that H2A.Z acetylation regulates neuronal fate specification by establishing epigenetic competence for bivalent gene activation and cell lineage transition.

Ferroptotic therapy in cancer: benefits, side effects, and risks.

Ferroptosis is a type of regulated cell death characterized by iron accumulation and uncontrolled lipid peroxidation, leading to plasma membrane rupture and intracellular content release. Originally investigated as a targeted therapy for cancer cells carrying oncogenic RAS mutations, ferroptosis induction now exhibits potential to complement chemotherapy, immunotherapy, and radiotherapy in various cancer types. However, it can lead to side effects, including immune cell death, bone marrow impairment, liver and kidney damage, cachexia (severe weight loss and muscle wasting), and secondary tumorigenesis. In this review, we discuss the advantages and offer an overview of the diverse range of documented side effects. Furthermore, we examine the underlying mechanisms and explore potential strategies for side effect mitigation.

Full-Spectrum Responsive Naphthalimide/Perylene Diimide with a Giant Internal Electric Field for Photocatalytic Overall Water Splitting.

The co-assembly naphthalimide/perylene diimide (NDINH/PDINH) supramolecular photocatalysts were successfully synthesized via a rapid solution dispersion method. A giant internal electric field (IEF) in co-assembly structure was built by the larger local dipole. NDINH coated on PDINH could reduce the reflected electric field over PDINH to improve its responsive activity to ultraviolet light. Resultantly, an efficient full-spectrum photocatalytic overall water splitting activity with H2 and O2 evolution rate of 317.2 and 154.8 µmol g-1 h-1 for NDINH/PDINH together with optimized O2 evolution rate with 2.61 mmol g-1 h-1 using AgNO3 as a sacrificial reagent were achieved. Meanwhile, its solar-to-hydrogen efficiency was enhanced to 0.13 %. The enhanced photocatalytic activity was primarily attributed to the IEF between NDINH and PDINH, significantly accelerating transfer and separation of photogenerated carriers. Additionally, a direct Z-Scheme pathway of carriers contributed to a high redox potential. The strategy provided a new perspective for the design of supramolecular photocatalysts.

Microvesicles from bone marrow-derived mesenchymal stem cells promote Helicobacter pylori-associated gastric cancer progression by transferring thrombospondin-2.

BACKGROUND: Our previous study found that bone marrow-derived mesenchymal stem cells (BMSCs) promote Helicobacter pylori (H pylori)-associated gastric cancer (GC) progression by secreting thrombospondin-2 (THBS2). Extracellular vesicles (EVs) are important carriers for intercellular communication, and EVs secreted by BMSCs have been shown to be closely related to tumor development. The aim of this study was to investigate whether BMSC-derived microvesicles (MVs, a main type of EV) play a role in H. pylori-associated GC by transferring THBS2. METHODS: BMSCs and THBS2-deficient BMSCs were treated with or without the supernatant of H. pylori for 12 h at a multiplicity of infection of 50, and their EVs were collected. Then, the effects of BMSC-derived MVs and THBS2-deficient BMSC-derived MVs on the GC cell line MGC-803 were assessed by in vitro proliferation, migration, and invasion assays. In addition, a subcutaneous xenograft tumor model, a nude mouse intraperitoneal metastasis model, and a tail vein injection metastasis model were constructed to evaluate the effects of BMSC-derived MVs and THBS2-deficient BMSC-derived MVs on GC development and metastasis in vivo. RESULTS: BMSC-derived MVs could be readily internalized by MGC-803 cells. BMSC-derived MVs after H. pylori treatment significantly promoted their proliferation, migration and invasion in vitro (all P < 0.05) and promoted tumor development and metastasis in a subcutaneous xenograft tumor model, a nude mouse intraperitoneal metastasis model, and a tail vein injection metastasis model in vivo (all P < 0.05). The protein expression of THBS2 was significantly upregulated after H. pylori treatment in BMSC-derived MVs (P < 0.05). Depletion of the THBS2 gene reduces the tumor-promoting ability of BMSC-MVs in an H. pylori infection microenvironment both in vitro and in vivo. CONCLUSION: Overall, these findings indicate that MVs derived from BMSCs can promote H. pylori-associated GC development and metastasis by delivering the THBS2 protein. Video Abstract.

Recognition of H3K9 methylation by GLP is required for efficient establishment of H3K9 methylation, rapid target gene repression, and mouse viability.

GLP and G9a are major H3K9 dimethylases and are essential for mouse early embryonic development. GLP and G9a both harbor ankyrin repeat domains that are capable of binding H3K9 methylation. However, the functional significance of their recognition of H3K9 methylation is unknown. Here, we report that the histone methyltransferase activities of GLP and G9a are stimulated by neighboring nucleosomes that are premethylated at H3K9. These stimulation events function in cis and are dependent on the H3K9 methylation binding activities of ankyrin repeat domains of GLP and G9a. Disruption of the H3K9 methylation-binding activity of GLP in mice causes growth retardation of embryos, ossification defects of calvaria, and postnatal lethality due to starvation of the pups. In mouse embryonic stem cells (ESCs) harboring a mutant GLP that lacks H3K9me1-binding activity, critical pluripotent genes, including Oct4 and Nanog, display inefficient establishment of H3K9me2 and delayed gene silencing during differentiation. Collectively, our study reveals a new activation mechanism for GLP and G9a that plays an important role in ESC differentiation and mouse viability.

Gastroenterologist-Level Identification of Small-Bowel Diseases and Normal Variants by Capsule Endoscopy Using a Deep-Learning Model.

BACKGROUND & AIMS: Capsule endoscopy has revolutionized investigation of the small bowel. However, this technique produces a video that is 8-10 hours long, so analysis is time consuming for gastroenterologists. Deep convolutional neural networks (CNNs) can recognize specific images among a large variety. We aimed to develop a CNN-based algorithm to assist in the evaluation of small bowel capsule endoscopy (SB-CE) images. METHODS: We collected 113,426,569 images from 6970 patients who had SB-CE at 77 medical centers from July 2016 through July 2018. A CNN-based auxiliary reading model was trained to differentiate abnormal from normal images using 158,235 SB-CE images from 1970 patients. Images were categorized as normal, inflammation, ulcer, polyps, lymphangiectasia, bleeding, vascular disease, protruding lesion, lymphatic follicular hyperplasia, diverticulum, parasite, and other. The model was further validated in 5000 patients (no patient was overlap with the 1970 patients in the training set); the same patients were evaluated by conventional analysis and CNN-based auxiliary analysis by 20 gastroenterologists. If there was agreement in image categorization between the conventional analysis and CNN model, no further evaluation was performed. If there was disagreement between the conventional analysis and CNN model, the gastroenterologists re-evaluated the image to confirm or reject the CNN categorization. RESULTS: In the SB-CE images from the validation set, 4206 abnormalities in 3280 patients were identified after final consensus evaluation. The CNN-based auxiliary model identified abnormalities with 99.88% sensitivity in the per-patient analysis (95% CI, 99.67-99.96) and 99.90% sensitivity in the per-lesion analysis (95% CI, 99.74-99.97). Conventional reading by the gastroenterologists identified abnormalities with 74.57% sensitivity (95% CI, 73.05-76.03) in the per-patient analysis and 76.89% in the per-lesion analysis (95% CI, 75.58-78.15). The mean reading time per patient was 96.6 ± 22.53 minutes by conventional reading and 5.9 ± 2.23 minutes by CNN-based auxiliary reading (P < .001). CONCLUSIONS: We validated the ability of a CNN-based algorithm to identify abnormalities in SB-CE images. The CNN-based auxiliary model identified abnormalities with higher levels of sensitivity and significantly shorter reading times than conventional analysis by gastroenterologists. This algorithm provides an important tool to help gastroenterologists analyze SB-CE images more efficiently and more accurately.

ESCRT-III-dependent membrane repair blocks ferroptosis.

Ferroptosis is a form of regulated cell death that is triggered by iron accumulation and lipid peroxidation. Although plasma membrane injuries represent an important event in cell death, the impact of membrane repair mechanisms on ferroptosis remains unidentified. Here, we provide the first evidence that membrane repair dependent on endosomal sorting complexes required for transport (ESCRT)-III negatively regulates ferroptotic cancer cell death. The accumulation of ESCRT-III subunits (e.g., CHMP5 and CHMP6) in the plasma membrane are increased by classical ferroptosis activators (e.g., erastin and RSL3), which relies on endoplasmic reticulum stress and calcium influx. Importantly, the knockdown of CHMP5 or CHMP6 by RNAi sensitizes human cancer cells (e.g., PANC1 and HepG2) to lipid peroxidation-mediated ferroptosis in vitro and in vivo. These findings suggest that ESCRT-III confers resistance to ferroptotic cell death, allowing cell survival under stress conditions.

Lipid storage and lipophagy regulates ferroptosis.

The synthesis, storage, and degradation of lipids are highly regulated processes. Impaired lipid metabolism is implicated in inflammation and cell death. Although ferroptosis is a recently described form of regulated cell death driven by lipid peroxidation, the impact of lipid droplets on ferroptosis remains unidentified. Here, we demonstrate that lipophagy, the autophagic degradation of intracellular lipid droplets, promotes RSL3-induced ferroptotic cell death in hepatocytes. Lipid droplet accumulation is increased at the early stage but decreased at the late stage of ferroptosis in mouse or human hepatocytes. Importantly, either genetically enhancing TPD52-dependent lipid storage or blocking ATG5-and RAB7A-dependent lipid degradation prevents RSL3-induced lipid peroxidation and subsequent ferroptosis in vitro and in vivo. These studies support an antioxidant role for lipid droplets in cell death and suggest novel strategies for the inhibition of ferroptosis by targeting the lipophagy pathway.

The value of combined vein resection in pancreaticoduodenectomy for pancreatic head carcinoma: a meta-analysis.

BACKGROUND: Although pancreaticoduodenectomy with vein resection (PDVR) is widely performed in selected patients with indications, its benefits remain controversial. In this meta-analysis, we evaluate the safety and efficacy of PDVR in comparison to standard pancreaticoduodenectomy (PD). METHODS: We searched PubMed, Embase, and Cochrane as well as the Chinese National Knowledge Infrastructure, Weipu, and Wanfang databases for studies that evaluate the value of PVDR. The data of the patients who underwent PD or PDVR were analyzed using Review Manager and STATA software. RESULTS: In comparison with the PD group, the PDVR group had a lower R0 resection rate and higher rates of complications such as biliary fistula, reoperation rate, delayed gastric emptying, cardiopulmonary abnormalities, hemorrhage, in-hospital mortality, 30-day mortality. The blood loss, duration of operation, total hospital stay is higher in PDVR group. CONCLUSIONS: Compared to standard PD, PDVR was associated with a greater risk of some specific complications and increase the mortality rate, total hospital stay time, combine with vein resection have a lower R0 resection rate. Therefore, combine with vascular resection for pancreatic cancer needs to be carefully selected by the surgeon.

Metal-organic frameworks/carbon-based materials for environmental remediation: A state-of-the-art mini-review.

In recent years, many research groups started to study the combination of metal-organic frameworks (MOFs) with nanocarbon materials, which showed the excellent improved performances than MOFs alone. The addition of carbon materials such as graphene oxides (GOs) and carbon nanotubes (CNTs) into MOFs can improve the physico-chemical properties of parent MOFs with excellent chemical robustness, high mechanical and distinguished electronic thermal robustness. These advantages facilitate the wider applications of MOFs/carbon materials (MOFs-C) in more research fields. This paper is devoted to reviewing the recent studies about the preparation and applications of MOFs-C in environmental remediation. This paper discusses the efficient adsorptive removal of a wide range of pollutants by MOFs-C, including organic contaminants and heavy metals from water as well as VOCs and some other toxic gases from atmospheric environment. Additionally, the catalytic performance of these nanocomposites for photocatalysis and Fenton-like oxidation of water pollutants is discussed in details. Meanwhile, the significant roles of nanocarbons and in-depth mechanisms for improved adsorption or catalysis are summarized. Finally, future perspectives on the development and application of MOFs-C composites for pollution remediation are presented at the end of this paper.

RIP3-mediated necrotic cell death accelerates systematic inflammation and mortality.

Systematic inflammation contributes to the development of many diseases, including cardiovascular disease, which is the leading cause of mortality worldwide. How such inflammation is initiated and maintained throughout the course of disease remains unclear. In the current study, we report the observation of specific phosphorylation of the receptor-interacting protein 3 (RIP3) kinase that marks the activation of programmed necrosis (also called the "necroptosis pathway") in the atherosclerotic plaques in apolipoprotein E (ApoE)-knockout mice. The mRNA expression levels of 10 inflammatory cytokines, including IL-1α, were decreased significantly in the plaque regions of mice lacking RIP3. Lymphocyte infiltrations in the adipocyte tissue and in skin lesions of ApoE single-knockout mice were significantly mitigated in ApoE/RIP3 double-knockout mice. The high percentage of inflammatory monocytes with high levels of lymphocyte antigen 6C in the blood of ApoE single-knockout mice also was greatly decreased in the ApoE/RIP3 double-knockout mice. Most significantly, the double-knockout mice displayed dramatically delayed mortality compared with ApoE single-knockout mice. Our findings indicate that necrotic death in areas such as atherosclerotic plaques may release cytokines that mobilize monocytes from bone marrow to the lesion sites, exacerbating the lesions in multiple tissues and resulting in the premature death of the animals.

Biological Decolorization and Degradation of Malachite Green by Pseudomonas sp. YB2: Process Optimization and Biodegradation Pathway.

A novel strain Pseudomonas sp. YB2, which was isolated from activated sludge, was studied for biological decolorization and degradation of malachite green (MG). The results show that this aerobic strain is an aerobic bacterium, which has relatively high salt tolerance and high antibiotic resistance. The optimal performance condition for both bacterial growth and decolorization of MG was at 25-35 °C and pH 5.0-7.0. It could efficiently decolorize 90.40% MG at a high concentration up to 1500 mg/L in 24 h, and concentrations of MG lower than 1000 mg/L could be completely decolorized in 12 h. The intermediate products of MG were detected using gas chromatography-mass spectrometer, including leucomalachite green, 4,4'-bis(dimethylamino) benzophenone, 4-(dimethylamino) benzophenone, phenol, dimethylaniline. The possible degradation pathways of MG by strain YB2 were proposed. This strain might be potentially useful for biodegradation of MG in real environments.

Nucleostemin and GNL3L exercise distinct functions in genome protection and ribosome synthesis, respectively.

The mammalian nucleolar proteins nucleostemin and GNL3-like (GNL3L) are encoded by paralogous genes that arose from an ancestral invertebrate gene, GNL3. Invertebrate GNL3 has been implicated in ribosome biosynthesis, as has its mammalian descendent, GNL3L. The paralogous mammalian nucleostemin protein has, instead, been implicated in cell renewal. Here, we found that depletion of nucleostemin in a human breast carcinoma cell line triggers prompt and significant DNA damage in S-phase cells without perturbing the initial step of ribosomal (r)RNA synthesis and only mildly affects the total ribosome production. By contrast, GNL3L depletion markedly impairs ribosome production without inducing appreciable DNA damage. These results indicate that, during vertebrate evolution, GNL3L retained the role of the ancestral gene in ribosome biosynthesis, whereas the paralogous nucleostemin acquired a novel genome-protective function. Our results provide a coherent explanation for what had seemed to be contradictory findings about the functions of the invertebrate versus vertebrate genes and are suggestive of how the nucleolus was fine-tuned for a role in genome protection and cell-cycle control as the vertebrates evolved.

RIP3-dependent necrosis induced inflammation exacerbates atherosclerosis.

Atherothrombotic vascular disease is already the leading cause of mortality worldwide. Atherosclerosis shares features with diseases caused by chronic inflammation. More attention should concentrates on the innate immunity effect atherosclerosis progress. RIP3 (receptor-interacting protein kinase 3) act through the transcription factor named Nr4a3 (Nuclear orphan receptors) to regulate cytokine production. Deletion RIP3 decreases IL-1α production. Injection of anti-IL-1α antibody protects against the progress of atherosclerosis in ApoE -/- mice. RIP3 as a molecular switch in necrosis, controls macrophage necrotic death caused inflammation. Inhibiting necrosis will certainly reduce atherosclerosis through limit inflammation. Necrotic cell death caused systemic inflammation exacerbated cardiovascular disease. Inhibition of necrosis may yield novel therapeutic targets for treatment in years to come.

Nucleostemin deletion reveals an essential mechanism that maintains the genomic stability of stem and progenitor cells.

Stem and progenitor cells maintain a robust DNA replication program during the tissue expansion phase of embryogenesis. The unique mechanism that protects them from the increased risk of replication-induced DNA damage, and hence permits self-renewal, remains unclear. To determine whether the genome integrity of stem/progenitor cells is safeguarded by mechanisms involving molecules beyond the core DNA repair machinery, we created a nucleostemin (a stem and cancer cell-enriched protein) conditional-null allele and showed that neural-specific knockout of nucleostemin predisposes embryos to spontaneous DNA damage that leads to severe brain defects in vivo. In cultured neural stem cells, depletion of nucleostemin triggers replication-dependent DNA damage and perturbs self-renewal, whereas overexpression of nucleostemin shows a protective effect against hydroxyurea-induced DNA damage. Mechanistic studies performed in mouse embryonic fibroblast cells showed that loss of nucleostemin triggers DNA damage and growth arrest independently of the p53 status or rRNA synthesis. Instead, nucleostemin is directly recruited to DNA damage sites and regulates the recruitment of the core repair protein, RAD51, to hydroxyurea-induced foci. This work establishes the primary function of nucleostemin in maintaining the genomic stability of actively dividing stem/progenitor cells by promoting the recruitment of RAD51 to stalled replication-induced DNA damage foci.

Oridonin attenuated human PC-3 cell activity by modulating the Wnt/ß-catenin signaling.

BACKGROUND: Prostate cancer (PC) prevention is effectively achieved through its inhibition. Oridonin (ORD), an active diterpenoid isolated from Rabdosia rubescens, has been shown to have an inhibitory effect on PC cells, although its impact on PC is unknown. OBJECTIVES: The present work investigated the actions and probable mechanisms of ORD on cellular proliferation, apoptosis, PC, and the wingless-type MMTV integration site family member 2 (Wnt)/ß-catenin signaling pathway using the androgen-independent PC-3 cell line. MATERIAL AND METHODS: In this study, cell viability was analyzed with MTT assay method, apoptotic morphology determined using DAPI dye method, while protein (CD1333, OCT-4, Nanog, SOX-2 & Aldh1A1) and mRNA expressions were analyzed with western blotting and real time polymerase chain reaction (PCR). RESULTS: We demonstrated a concentration-dependent ORD inhibition of PC-3 cell proliferation and inhibition of induction apoptosis. Furthermore, ORD decreased PC-3 Wnt-2, phosphorylated glycogen synthase kinase-3 (p-GSK3), and ß-catenin protein levels and downregulated cyclin-D1 and c-myc messenger ribonucleic acid (mRNA). CONCLUSIONS: Oridonin inhibited proliferation and induced apoptosis in PC-3 cells, with the findings suggesting that it acted via the Wnt/ß-catenin pathway to exert its effects. This study demonstrates that ORD may impact PC.

Nucleostemin inhibits TRF1 dimerization and shortens its dynamic association with the telomere.

TRF1 is a key component of the telomere-capping complex and binds double-strand telomeric DNA as homodimers. So far, it is not clear whether TRF1 dimerization coincides with its telomere binding or is actively controlled before it binds the telomere, and in the latter case, how this event might affect its telomere association. We previously found that TRF1 dimerization and its telomere binding can be increased by GNL3L, which is the vertebrate paralogue of nucleostemin (NS). Here, we show that NS and GNL3L bind TRF1 directly but competitively through two separate domains of TRF1. In contrast to GNL3L, NS prevents TRF1 dimerization through a mechanism not determined by its ability to displace TRF1-bound GNL3L. Furthermore, NS is capable of shortening the dynamic association of TRF1 with the telomere in normal and TRF2(ΔBΔM)-induced telomere-damaged cells without affecting the amount of telomere-bound TRF1 proteins in vivo. Importantly, NS displays a protective function against the formation of telomere-dysfunction-induced foci. This work demonstrates that TRF1 dimerization is actively and oppositely regulated by NS and GNL3L extrachromosomally. Changing the relative amount of TRF1 monomers versus dimers in the nucleoplasm might affect the dynamic association of TRF1 with the telomere and the repair of damaged telomeres.

Chromatin-modifying enzymes as modulators of nuclear size during lineage differentiation.

The mechanism of nuclear size determination and alteration during normal lineage development and cancer pathologies which is not fully understood. As recently reported, chromatin modification can change nuclear morphology. Therefore, we screened a range of pharmacological chemical compounds that impact the activity of chromatin-modifying enzymes, in order to get a clue of the specific types of chromatin-modifying enzymes that remarkably effect nuclear size and shape. We found that interrupted activity of chromatin-modifying enzymes is associated with nuclear shape abnormalities. Furthermore, the activity of chromatin-modifying enzymes perturbs cell fate determination in cellular maintenance and lineage commitment. Our results indicated that chromatin-modifying enzyme regulates cell fate decision during lineage differentiation and is associate with nuclear size alteration.

Significant correlation between glucose metabolism status and acute radiation enteritis resulting from concurrent chemoradiotherapy in rectal cancer.

OBJECTIVE: To explore the relationship between glucose metabolism and acute radiation enteritis from chemoradiotherapy for rectal cancer. METHODS: In this retrospective study, the clinical data of 75 rectal cancer patients who received concurrent chemoradiotherapy in Binzhou Second People's Hospital from February 2019 to February 2022 were collected and analyzed. According to the Radiation Therapy Oncology Group (RTOG)/European Organization for Research on Treatment of Cancer (EORTC) radiation response grading criteria, the patients were classified into four groups with different glucose metabolism statuses: NGR (normal glucose regulation) group, IFG (impaired fasting glucose) group, IGT (impaired glucose tolerance) group, and DM (diabetes mellitus) group. Two-factor logistic regression was used to analyze whether IFG, IGT, or DM were risk factors for acute radiation enteritis. RESULTS: (1) The fasting plasma glucose (FPG, F=20.550, P < 0.001), 2-hour post-meal blood glucose (2hPG, F=14.920, P < 0.001), triglycerides (TG, F=3.355, P=0.024), high-density lipoprotein cholesterol (HDL-C) (F=4.109, P=0.010), low-density lipoprotein cholesterol (LDL-C, F=4.545, P=0.006), and systolic blood pressure (SBP, F=5.398, P=0.002) differed greatly among the NGR group, IFG group, IGT group, and DM group, all P < 0.05. (2) The incidence of acute radiation enteritis was 34.67% in the 75 patients, and in DM patients it was higher than in the NGR, IFG, or IGT patients (χ2=14.702, P=0.002). (3) There were significant differences in BMI (F=3.594, P=0.044) and DBP (F=3.954, P=0.033) among the asymptomatic group, mild group, and severe group (P < 0.05). (4) Body mass index (BMI) was positively correlated with acute radiation enteritis in IFG, IGT, and DM patients (OR=1.361, P=0.020). (5) DM was positively correlated with acute radiation enteritis (OR=6.167, P=0.039). CONCLUSIONS: DM was significantly correlated with acute radiation enteritis induced by concurrent chemoradiotherapy for rectal cancer, while IFG and IGT were not.

Z-scheme plasmonic Ag decorated Bi2WO6/NiO hybrids for enhanced photocatalytic treatment of naphthenic acids in real oil sands process water under simulated solar irradiation.

A novel photocatalyst, Bi2WO6/NiO/Ag, with hierarchical flower-like Z-scheme heterojunction, which exhibited excellent stability and photocatalytic activity over a wide light spectrum, was firstly synthesized and used in the remediation of real oil sands process water (OSPW) and achieved complete removal of aromatics, classical naphthenic acids (NAs), and heteroatomic NAs after 6 h of photocatalytic treatment. The acute toxicity of OSPW was completely eliminated after only 2 h of treatment. h+ and ∙OH were found to be the major oxidative species in the photocatalytic system. The enhanced photocatalytic efficiency is the result of the unique Z-scheme electron transfer among electron mediators Ag, NiO, and Bi2WO6, which was supported by the in-situ irradiated XPS. The study benefits the design of engineered passive treatment approach for OSPW remediation through solar light-driven catalyst.