Genome-scale CRISPR-Cas9 screen identifies PAICS as a therapeutic target for EGFR wild-type non-small cell lung cancer.

Epidermal growth factor receptor-targeted (EGFR-targeted) therapies show promise for non-small cell lung cancer (NSCLC), but they are ineffective in a third of patients who lack EGFR mutations. This underlines the need for personalized treatments for patients with EGFR wild-type NSCLC. A genome-wide CRISPR/Cas9 screen has identified the enzyme phosphoribosylaminoimidazole carboxylase/phosphoribosylaminoimidazole succinocarboxamide synthetase (PAICS), which is vital in de novo purine biosynthesis and tumor development, as a potential drug target for EGFR wild-type NSCLC. We have further confirmed that PAICS expression is significantly increased in NSCLC tissues and correlates with poor patient prognosis. Knockdown of PAICS resulted in a marked reduction in both in vitro and in vivo proliferation of EGFR wild-type NSCLC cells. Additionally, PAICS silencing led to cell-cycle arrest in these cells, with genes involved in the cell cycle pathway being differentially expressed. Consistently, an increase in cell proliferation ability and colony number was observed in cells with upregulated PAICS in EGFR wild-type NSCLC. PAICS silencing also caused DNA damage and cell-cycle arrest by interacting with DNA repair genes. Moreover, decreased IMPDH2 activity and activated PI3K-AKT signaling were observed in NSCLC cells with EGFR mutations, which may compromise the effectiveness of PAICS knockdown. Therefore, PAICS plays an oncogenic role in EGFR wild-type NSCLC and represents a potential therapeutic target for this disease.

Metabolic perturbation of Streptomyces albulus by introducing NADP-dependent glyceraldehyde 3-phosphate dehydrogenase.

The available resources of Streptomyces represent a valuable repository of bioactive natural products that warrant exploration. Streptomyces albulus is primarily utilized in the industrial synthesis of ε-poly-L-lysine (ε-PL). In this study, the NADP-dependent glyceraldehyde 3-phosphate dehydrogenase (GapN) from Streptococcus mutans was heterologously expressed in S. albulus CICC11022, leading to elevated intracellular NADPH levels and reduced NADH and ATP concentrations. The resulting perturbation of S. albulus metabolism was comprehensively analyzed using transcriptomic and metabolomic methodologies. A decrease in production of ε-PL was observed. The expression of gapN significantly impacted on 23 gene clusters responsible for the biosynthesis of secondary metabolites. A comprehensive analysis revealed a total of 21 metabolites exhibiting elevated levels both intracellularly and extracellularly in the gapN expressing strain compared to those in the control strain. These findings underscore the potential of S. albulus to generate diverse bioactive natural products, thus offering valuable insights for the utilization of known Streptomyces resources through genetic manipulation.

miR-223-3p Prevents Necroptotic Macrophage Death by Targeting Ripk3 in a Negative Feedback Loop and Consequently Ameliorates Advanced Atherosclerosis.

BACKGROUND: The formation of large necrotic cores results in vulnerable atherosclerotic plaques, which can lead to severe cardiovascular diseases. However, the specific regulatory mechanisms underlying the development of necrotic cores remain unclear. METHODS: To evaluate how the modes of lesional cell death are reprogrammed during the development of atherosclerosis, the expression levels of key proteins that are involved in the necroptotic, apoptotic, and pyroptotic pathways were compared between different stages of plaques in humans and mice. Luciferase assays and loss-of-function studies were performed to identify the microRNA-mediated regulatory mechanism that protects foamy macrophages from necroptotic cell death. The role of this mechanism in atherosclerosis was determined by using a knockout mouse model with perivascular drug administration and tail vein injection of microRNA inhibitors in Apoe-/- mice. RESULTS: Here, we demonstrate that the necroptotic, rather than the apoptotic or pyroptotic, pathway is more activated in advanced unstable plaques compared with stable plaques in both humans and mice, which closely correlates with necrotic core formation. The upregulated expression of Ripk3 (receptor-interacting protein kinase 3) promotes the C/EBPß (CCAAT/enhancer binding protein beta)-dependent transcription of the microRNA miR-223-3p, which conversely inhibits Ripk3 expression and forms a negative feedback loop to regulate the necroptosis of foamy macrophages. The knockout of the Mir223 gene in bone marrow cells accelerates atherosclerosis in Apoe-/- mice, but this effect can be rescued by Ripk3 deficiency or treatment with the necroptosis inhibitors necrostatin-1 and GSK-872. Like the Mir223 knockout, treating Apoe-/- mice with miR-223-3p inhibitors increases atherosclerosis. CONCLUSIONS: Our study suggests that miR-223-3p expression in macrophages protects against atherosclerotic plaque rupture by limiting the formation of necrotic cores, thus providing a potential microRNA therapeutic candidate for atherosclerosis.

Rab27a-mediated extracellular vesicle secretion contributes to osteogenesis in periodontal ligament-bone niche communication.

Periodontitis, an infectious and common disease worldwide, leads to the destruction of the periodontal ligament-alveolar bone complex. Within the bone metabolic niche, communication between periodontal ligament stem cells (PDLSCs) and bone marrow mesenchymal stem cells (BMMSCs) has been considered a major contributor to osteogenesis. PDLSC-derived extracellular vesicles (P-EVs) have shown great potential for bone regeneration. However, the secretion and uptake mechanisms of P-EVs remain elusive. Herein, the biogenesis of extracellular vesicles (EVs) from PDLSCs was observed using scanning and transmission electron microscopy. PDLSCs were transduced with Ras-associated protein 27a (Rab27a) siRNA (PDLSCsiRab27a) to inhibit EV secretion. The effect of P-EVs on BMMSCs was evaluated using a non-contact transwell co-culture system. We observed that Rab27a knockdown decreased EV secretion, and PDLSCsiRab27a remarkably attenuated co-culture-enhanced osteogenesis of BMMSCs. Isolated PDLSC-derived EVs enhanced osteogenic differentiation of BMMSCs in vitro and induced bone regeneration in a calvarial defect model in vivo. PDLSC-derived EVs were rapidly endocytosed by BMMSCs via the lipid raft/cholesterol endocytosis pathway and triggered the phosphorylation of extracellular signal-regulated kinase 1/2. In conclusion, PDLSCs contribute to the osteogenesis of BMMSCs through Rab27a-mediated EV secretion, thereby providing a potential cell-free approach for bone regeneration.

Distinct neural correlates of poor decoding and poor comprehension in children with reading disability.

Reading disability (RD) can manifest itself as a word decoding problem or a reading comprehension problem. In the current study, we identified 3 subtypes of RD: poor decoders (PD), poor comprehenders (PC), and poor-in-both (PB). We found that PD had greater deficits in meta-linguistic skills such as phonological awareness, orthographic skills, and morphological skills than PC, whereas PC had greater deficits in listening comprehension than PD. In the brain, we also found different patterns of deficits during an auditory rhyming judgment task using functional magnetic resonance imaging. PD showed less activation than PC and age controls in the left dorsal inferior frontal gyrus (IFG) and pre-supplementary motor area (SMA), brain activation of which was correlated with phonological awareness and working memory. In contrast, PC showed less activation in the left fusiform gyrus than PD and age controls, which was correlated with reading comprehension fluency and morphological skill. Last, PB showed both PD's and PC's deficits, as well as additional deficits in the bilateral lingual gyri. Our findings contribute to revealing different neural signatures of poor decoding and poor comprehension, which are distinct disorders but co-occur very often. These findings implicate possibility and necessity of precise diagnosis and individualized intervention.

Chronic intermittent hypoxia impaired collagen synthesis in mouse genioglossus via ROS accumulation: A transcriptomic analysis.

Obstructive sleep apnea (OSA) is a sleep-related breathing disorder characterized by intermittent and recurrent upper airway collapse during sleep that leads to chronic intermittent hypoxia (CIH). The genioglossus (GG) is the largest dilator muscle, which controls the upper airway and plays an important role in OSA pathology. Elucidating its genetic alterations may help identify potential targets for OSA. However, the genetic aspects of the GG in CIH mice remain unclear. Here, we have conducted an RNA sequencing (RNA-Seq) analysis to assess the differentially expressed genes (DEGs) in the GG between CIH mice and normoxia (NOR) mice. A total of 637 DEGs were identified to be dysregulated in CIH mice compared with control mice. Bioinformatics analysis showed that the DEGs were related to various physiological processes, such as the endogenous stimulus responses, cellular component organization and metabolic processes. Extracellular matrix (ECM)-receptor interaction was the top KEGG pathway in the environmental information processing category with high significance and large fold changes. From the gene weight distributions of collagen (Col)-related biological processes (BPs), we found several significant DEGs, such as Col1a1, Col1a2, Mmp2, Col3a1, Col5a1, Fmod, and Col5a2. A PPI network showed that Col1a1 was linked to ECM-receptor interactions, responses to reactive oxygen species (ROS) and Col-related BPs. It was verified in vivo and in vitro that hypoxia can induce excess ROS and reduce Col expression levels. Moreover, we found NAC can effectively scavenge ROS and restore collagen synthesis. These findings contribute to a better understanding of the mechanisms linking OSA and upper airway muscle injury and may help identify potential therapeutic targets.

Transcriptomic and metabolomic analyses for providing insights into the influence of polylysine synthetase on the metabolism of Streptomyces albulus.

ε-poly-L-lysine (ε-PL) is the main secondary metabolite of Streptomyces albulus, and it is widely used in the food industry. Polylysine synthetase (Pls) is the last enzyme in the ε-PL biosynthetic pathway. Our previous study revealed that Pls overexpressed in S. albulus CICC11022 result in the efficient production of ε-PL. In this study, a Pls gene knockout strain was initially constructed. Then, genomic, transcriptomic and metabolomic approaches were integrated to study the effects of the high expression and knockout of Pls on the gene expression and metabolite synthesis of S. albulus. The high expression of Pls resulted in 598 significantly differentially expressed genes (DEGs) and 425 known differential metabolites, whereas the inactivation of Pls resulted in 868 significant DEGs and 374 known differential metabolites. The expressions of 8 and 35 genes were negatively and positively associated with the Pls expression, respectively. Subsequently, the influence mechanism of the high expression and inactivation of Pls on the ε-PL biosynthetic pathway was elucidated. Twelve metabolites with 30% decreased yield in the high-expression strain of Pls but 30% increased production in the Pls knockout strain were identified. These results demonstrate the influence of Pls on the metabolism of S. albulus. The present work can provide the theoretical basis for improving the production capacity of ε-PL by means of metabolic engineering or developing bioactive substances derived from S. albulus.

Genome-wide CRISPR/Cas9 screening for therapeutic targets in NSCLC carrying wild-type TP53 and receptor tyrosine kinase genes.

BACKGROUND: Targeted drugs have greatly improved the therapeutic outcome of non-small cell lung cancer (NSCLC) patients compared with conventional chemotherapy, whereas about one-third of patients are so far not suitable for targeted therapy due to lack of known driver oncogenes such as a mutated receptor tyrosine kinase (RTK) genes. In this study, we aimed to identify therapeutic targets for this subgroup of NSCLC patients. METHODS: We performed genome-wide CRISPR/Cas9 screens in two NSCLC cell lines carrying wild-type TP53 and receptor tyrosine kinase (wtTP53-RTK) genes using a GeCKO v2.0 lentiviral library (containing 123411 sgRNAs and targeting 19050 genes). MAGeCKFlute was used to analyse and identify candidate genes. Genetic perturbation and pharmacological inhibition were used to validate the result in vitro and in vivo. RESULTS: The Genome-wide CRISPR/Cas9 screening identified MDM2 as a potential therapeutic target for wtTP53-RTK NSCLC. Genetic and pharmacological inhibition of MDM2 reduced cell proliferation and impaired tumour growth in the xenograft model, thus confirming the finding of the CRISPR/Cas9 screening. Moreover, treatment by a selective MDM2 inhibitor RG7388 triggered both cell cycle arrest and apoptosis in several NSCLC cell lines. Additionally, RG7388 and pemetrexed synergistically blocked the cell proliferation and growth of wtTP53-RTK tumours but had limited effects for other genotypes. CONCLUSIONS: We identified MDM2 as an essential gene and a potential therapeutic target in wtTP53-RTK NSCLC via a genome-wide CRISPR/Cas9 screening. For this subgroup, treatment by RG7388 alone or by its combination with pemetrexed resulted in significant tumour inhibition.

[Salidroside inhibits phenotypic transformation of rat pulmonary artery smooth muscle cells induced by hypoxia].

This study investigated the effect of salidroside on phenotypic transformation of rat pulmonary artery smooth muscle cells(PASMCs) induced by hypoxia. Rat pulmonary arteries were isolated by tissue digestion and PASMCs were cultured. The OD values of cells treated with salidroside at different concentrations for 48 hours were measured by cell counting kit-8(CCK-8) to determine the appropriate concentration range of salidroside. The cells were divided into a normal(normoxia) group, a model(hypoxia) group, and three hypoxia + salidroside groups(40, 60, and 80 µg·mL~(-1)). Quantitative real-time PCR(qRT-PCR) was used to detect the mRNA expression of cell contractile markers in each group, such as α-smooth muscle actin(α-SMA), smooth muscle 22(SM22), and calcium-binding protein(calponin), and synthetic marker vimentin. The expression levels of cell phenotypic markers and proliferating cell nuclear antigen(PCNA) were detected by Western blot. The proliferation of cells in each group was detected by the 5-ethynyl-2'-deoxyuridine(EdU) assay. Cell migration was measured by Transwell assay. As revealed by results, compared with the normal group, the model group showed decreased mRNA and protein expression of contractile phenotypic markers of PASMCs and increased mRNA and protein expression of synthetic markers. Compared with the conditions in the model group, salidroside could down-regulate the mRNA and protein expression of synthetic markers in PASMCs and up-regulated the mRNA and protein expression of contractile phenotypic markers. Compared with the normal group, the model group showed potentiated proliferation and migration. Compared with the model group, the hypoxia + salidroside groups showed blunted proliferation and migration of cells after phenotypic transformation. The results suggest that salidroside can inhibit the expression of synthetic markers in PASMCs and promote the expression of contractile markers to inhibit the hypoxia-induced phenotypic transformation of PASMCs. The mechanism of salidroside in inhibiting the proliferation and migration of PASMCs is related to the inhibition of the phenotypic transformation of PASMCs.

Periodontal Ligament Stem Cell-Derived Small Extracellular Vesicles Embedded in Matrigel Enhance Bone Repair Through the Adenosine Receptor Signaling Pathway.

PURPOSE: Small extracellular vesicles (sEVs) are natural biocarriers for biomolecule transfer between cells and promising therapeutic strategies for bone defect repair. In this study, human periodontal ligament stem cell (PDLSC)-derived sEVs (P-EVs) were immobilized in Matrigel to establish a topical cell-free transplantation strategy for bone repair. METHODS: PDLSCs were cultured and P-EVs were isolated from the culture supernatant. In a rat bilateral calvarial defect model, P-EV/Matrigel was plugged into one defect and PBS/Matrigel was applied to the other. Bone repair in vivo was assessed by micro-computed tomography, histomorphometry, and immunohistochemical staining. In vitro, we investigated the effects of P-EVs on the proliferation and migration capabilities of bone marrow mesenchymal stem cells (BMMSCs) and explored the potential mechanism of action. RESULTS: The in vivo study showed that P-EV/Matrigel accelerated bone tissue repair by increasing cell infiltration when compared with the control. In vitro, P-EVs enhanced proliferation and migration of BMMSCs via increased phosphorylation of AKT and extracellular signal-regulated kinase 1/2 (ERK1/2). The role of P-EV-induced adenosine receptor signaling in AKT and ERK1/2 phosphorylation was a key mediator during enhanced BMMSC migration. CONCLUSION: These results are the first to demonstrate that P-EVs accelerated the repair of bone defects, partially through promoting cell proliferation and migration. P-EV/Matrigel, which combines topical EV-implantation and extracellular matrix scaffolds, provides a new cell-free strategy for bone tissue repair.

Simultaneous Detoxification of Aflatoxin B1, Zearalenone and Deoxynivalenol by Modified Montmorillonites.

Raw Ca-based montmorillonite (MMT) was treated by H2SO4, calcination and organic compounds (hexadecyltrimethyl ammonium bromide (HTAB), cetylpyridinium chloride (CPC) and chitosan (CTS)), respectively. The modified montmorillonites were characterized by different methods and their adsorption performances for three mycotoxins (Aflatoxin B1 (AFB1), zearalenone (ZEA) and deoxynivalenol (DON)) were evaluated at pH = 2.8 and 8.0, respectively. The results indicate that surfactants (CPC and HTAB) intercalation is the most efficient modification, which obviously improves the adsorption performance of montmorillonite for mycotoxins, with adsorption efficiency of above 90% for AFB1 and ZEA whether under acid or alkaline conditions, due to the increase in basal spacing and the improvement of hydrophobicity. Moreover, the adsorption efficiencies of AFB1 and ZEA over CPC-modified montmorillonite (CPC-AMMT-3) coexisting with vitamin B6 or lysine are still at a high level (all above 94%). All modified montmorillonites, however, have low adsorption efficiency for DON, with somewhat spherical molecular geometry.

Childhood Maltreatment, Automatic Negative Thoughts, and Resilience: The Protective Roles of Culture and Genes.

Resilience, a psychological trait conceptualized as the ability to recover from setbacks, can be weakened by childhood maltreatment, which comprises childhood abuse and childhood neglect. The current study aimed to investigate whether childhood maltreatment could increase automatic negative thoughts (ANT), thus weakening resilience. Furthermore, as psychological characteristics are commonly subject to the moderating effects of cultural context and biology, the study also explored whether and how cultural and genetic factors separately interact with childhood maltreatment to predict resilience. In study 1, the participants comprised 237 American and 347 Chinese individuals; study 2 included 428 genotyped Chinese individuals. We combined regression, mediation, moderation, and machine learning methods to test the mediating effect of ANT on the link between childhood maltreatment and resilience as well as the moderating roles of culture and genetics. Study 1 found that both childhood abuse and childhood neglect increased ANT and thus weakened resilience. In addition, the ANT-mediating effects of childhood neglect were stronger in American than Chinese participants. In Study 2, using the leave-one-out approach, we constructed two separate prediction models based on 22 and 16 important single nucleotide polymorphisms (SNPs), and we found that the interaction between childhood abuse/neglect and polygenic scores based on important SNPs could predict ANT. The mediating effects of ANT on the relationship between childhood abuse/neglect and resilience were significant for participants with low polygenic scores but not for those with high polygenic scores. In conclusion, both the cultural environment and individual genetic makeup moderated the mediating effects of ANT on the association between childhood maltreatment and resilience. These findings indicated the roles of culture and genetics in protecting against the adverse effects of childhood maltreatment on resilience.

Research progress on the mechanism of phenotypic transformation of pulmonary artery smooth muscle cells induced by hypoxia.

Phenotypic transformation of pulmonary artery smooth muscle cells (PASMCs) is a key factor in pulmonary vascular remodeling. Inhibiting or reversing phenotypic transformation can inhibit pulmonary vascular remodeling and control the progression of hypoxic pulmonary hypertension. Recent studies have shown that hypoxia causes intracellular peroxide metabolism to induce oxidative stress, induces multi-pathway signal transduction, including those related to autophagy, endoplasmic reticulum stress and mitochondrial dysfunction, and also induces non-coding RNA regulation of cell marker protein expression, resulting in PASMCs phenotypic transformation. This article reviews recent research progress on mechanisms of hypoxia-induced phenotypic transformation of PASMCs, which may be helpful for finding targets to inhibit phenotypic transformation and to improve pulmonary vascular remodeling diseases such as hypoxia-induced pulmonary hypertension.

Poor reading is characterized by a more connected network with wrong hubs.

Using graph theory, we examined topological organization of the language network in Chinese children with poor reading during an auditory rhyming task and a visual spelling task, compared to reading-matched controls and age-matched controls. First, poor readers (PR) showed reduced clustering coefficient in the left inferior frontal gyrus (IFG) and higher nodal efficiency in the bilateral superior temporal gyri (STG) during the visual task, indicating a less functionally specialized cluster around the left IFG and stronger functional links between bilateral STGs and other regions. Furthermore, PR adopted additional right-hemispheric hubs in both tasks, which may explain increased global efficiency across both tasks and lower normalized characteristic shortest path length in the visual task for the PR. These results underscore deficits in the left IFG during visual word processing and conform previous findings about compensation in the right hemisphere in children with poor reading.

Downregulated hypoxia-inducible factor 1α improves myoblast differentiation under hypoxic condition in mouse genioglossus.

The treatment of obstructive sleep apnea-hypopnea syndrome targets the narrow anatomic structure of the upper airway (UA) and lacks an effective therapy for UA dilator muscle dysfunction. Long-term hypoxia can cause damage to UA dilator muscles and trigger a vicious cycle. We previously confirmed that hypoxia-inducible factor 1α (HIF-1α) upregulation mediates muscle fatigue in hypoxia condition, but the underlying mechanism remains to be determined. The present study investigated the intrinsic mechanisms and related pathways of HIF-1α that affect myoblast differentiation, with an aim to search for compounds that have protective effects in hypoxic condition. Differentiation of myoblasts was induced under hypoxia, and we found that hypoxia significantly inhibits the differentiation of myoblasts, damages the ultrastructure of mitochondria, and reduces the expression of myogenin, PGC-1ß and pAMPKα1. HIF-1α has a negative regulation effect on AMPK. Downregulation of HIF-1α increases the expression of the abovementioned proteins, promotes the differentiation of myoblasts, and protects mitochondrial integrity. In addition, mitochondrial biogenesis occurs during myogenic differentiation. Inhibition of the AMPK pathway inhibits mitochondrial biogenesis, decreases the level of PGC-1ß, and increases apoptosis. Resveratrol dimer can reverse the mitochondrial damage induced by AMPK pathway inhibition and decrease myoblast apoptosis. Our results provided a regulatory mechanism for hypoxic injury in genioglossus which may contribute to the pathogenesis and treatment of OSAHS.

Effect of acid-treated and hexadecyltrimethylammonium bromide-modified montmorillonites on adsorption performance of mycotoxins.

A series of modified montmorillonites treated by acid and hexadecyltrimethylammonium bromide (HTAB) were prepared and characterized, and their adsorption performances for three mycotoxins (aflatoxin B1, zearalenone, and deoxynivalenol) were evaluated at pH 2.8 and 8.0, respectively. The results indicate that the layers of raw montmorillonite are exfoliated after acid treatment and more active sites for adsorption of weak polar mycotoxins are exposed. While the intercalation of HTAB leads to an obvious increase of the interlamellar spacing and hydrophobic character of montmorillonite. The HTAB-AMMT-3 modified by acid and HTAB exhibits excellent adsorption capacity towards aflatoxin B1 (AFB1) and zearalenone (ZEA) whether in acidic or alkaline conditions compared with raw montmorillonite (MMT). However, all modified montmorillonites have low adsorption capacity for DON due to its poor planarity preventing it from entering into interfacial layer of montmorillonite.

Hypoxia-Induced ROS Contribute to Myoblast Pyroptosis during Obstructive Sleep Apnea via the NF-κB/HIF-1α Signaling Pathway.

Tissue hypoxia caused by upper airway collapse is a main cause of excessive oxidative stress and systemic inflammation in obstructive sleep apnea (OSA) patients. Increased reactive oxygen species (ROS) and inflammatory responses affect cell survival and ultimately contribute to tissue injury. In the present study, we proposed that the induction of ROS by hypoxia, as an intrinsic stress, activates myoblast pyroptosis in OSA. We found increased cell death and abnormal expression of pyroptosis markers in the skeletal muscle of OSA mice. In vitro studies showed hypoxia-induced pyroptotic death of C2C12 myoblasts, as evidenced by the activation of caspase-1 and gasdermin D (GSDMD). Hypoxia induced ROS overproduction and accumulation in myoblasts. More importantly, applying N-acetylcysteine (NAC), an ROS scavenger, rescued cell swelling, downregulated the inflammatory response, and prevented pyroptotic death in hypoxia-cultured myoblasts. Hypoxia stimulation promoted NF-κB P65 phosphorylation and HIF-1α nuclear translocation. Moreover, hypoxia increased the nuclear level of cleaved caspase-1 and GSDMD. NAC inhibited hypoxia-induced variations in the HIF-1α and NF-κB signaling pathway. Taken together, our results determined that hypoxia-induced ROS contribute to myoblast pyroptosis. Therefore, our findings suggest that ROS may be a potential therapeutic target for ameliorating hypoxia-induced cell death and tissue injury, especially in OSA and hypoxia-related diseases.

Promoting effect of Nb doping on catalytic performance for deep oxidation of 1, 2-dichloroethane over (Ce,Cr)xO2-Nb2O5 catalysts.

A series of Nb-doped (Ce,Cr)xO2-Nb2O5 mixed oxides with varying (Ce,Cr)xO2/Nb2O5 mass ratio were prepared by a co-precipitation method and evaluated for the catalytic performance of eliminating 1,2-dichloroethane (DCE). The results indicate that there exists a strong synergistic effect between acid sites and redox species in (Ce,Cr)xO2-Nb2O5 improving the catalytic activity for DCE oxidation. Appropriate Nb doping could promote the high dispersion and the interaction of metal oxides in the (Ce,Cr)xO2-Nb2O5 catalysts, resulting in the formation of more Cr6+ species with strong oxidizing ability and excellent mobility of oxygen species from bulk to surface to create more active sites for DCE deep oxidation. The (Ce,Cr)xO2-Nb2O5 catalysts with (Ce,Cr)xO2/Nb2O5 ratios of 2/1~1/2 exhibit excellent catalytic activity and durability for DCE degradation in dry air as well as benzene or water vapor, and less chlorinated byproduct is produced during the degradation of DCE.