Lipid-lowering, antihypertensive, and antithrombotic effects of nattokinase combined with red yeast rice in patients with stable coronary artery disease: a randomized, double-blinded, placebo-controlled trial.

Nattokinase (NK) and red yeast rice (RYR) are both indicated for their potential in cardiovascular disease prevention and management, but their combined effects especially in coronary artery disease (CAD) are scarcely examined. This 90-day randomized, double-blind trial aims to investigate the effect of NK and RYR supplementations on cardiometabolic parameters in patients with stable CAD. 178 CAD patients were randomized to four groups: NK + RYR, NK, RYR, and placebo. No adverse effects due to the interventions were reported. In comparisons across groups, NK + RYR showed the maximum effect in reducing triglyceride (-0.39 mmol), total cholesterol (-0.66 mmol/L), diastolic blood pressure (-7.39 mmHg), and increase in high-density lipoprotein cholesterol (0.195 mmol/L) than other groups (all p for multiple groups comparison<0.01). Both NK + RYR and NK groups had significantly better-improved lactate dehydrogenase than the others (-29.1 U/L and - 26.4 U/L). NK + RYR group also showed more potent reductions in thromboxane B2 and increases in antithrombin III compared to placebo (both p < 0.01). These improved markers suggest that combined NK and RYR may preferably alter antithrombin and COX-1 pathways, potentially reducing thrombosis risks in CAD patients. Overall, the combined NK and RYR supplementation is safe and more effective than separately in improving cardiometabolic markers among CAD patients with multiple heart medications use.

Comparison of Laminectomy with Fusion and Laminoplasty Treating Multilevel Cervical Spondylotic Myelopathy: A Single-Center Retrospective Study.

OBJECTIVE: Comparing laminectomy with fusion (LF) and laminoplasty (LP) for treating multilevel cervical spondylotic myelopathy (MCSM) and comparative analysis of neck pain and sagittal cervical parameters. METHODS: This single-center study retrospectively analyzed MCSM patients treated with LF or LP in our department between June 2018 and January 2023, with at least a 12-month follow-up. T-tests were used to identify operation time, hemoglobin, hospital stay, modified Japanese Orthopaedic Association (mJOA) score, C2-C7 Cobb angle, C2-C7 sagittal vertical axis, T1 slope, cervical range of motion (cROM), and C4/5 anterior and posterior spinal canal diameter (A-P diameter) and area. Nonparametric tests were used to identify visual analog scale (VAS) score (assessing neck pain). Pearson correlation analyses were used to identify the neck pain. RESULTS: Of all 67 patients (LF: 24, LP: 43), both groups' mJOA scores significantly improved (P < 0.001). The VAS scores had both significantly decreased, with the LF group exhibiting a more marked reduction (LF: P < 0.001, LP: P = 0.037). Both groups' C4/5 A-P diameters and areas increased significantly (P < 0.001). The cROM had both significantly decreased, with the LF group exhibiting a greater reduction. At the last follow-up, the LF group's T1 slope and C2-C7 Cobb angle considerably increased, and pain VAS scores substantially correlated with the C2-C7 Cobb angle (R = -0.451, P < 0.001). CONCLUSIONS: LF and LP were efficacious for MCSM. LF relieved neck pain better but caused greater reduction in cervical mobility. Cervical lordosis improvement was significantly correlated with neck pain alleviation.

Comparison of anterior cervical diskectomy with fusion (ACDF) and laminoplasty treating multilevel cervical spondylotic myelopathy with developmental canal stenosis: a retrospective study.

PURPOSE: To evaluate clinical effectiveness and radiologic results of anterior cervical diskectomy with fusion (ACDF) comparing with laminoplasty (LP) in treating multilevel cervical spondylotic myelopathy (MCSM) with developmental canal stenosis (DCS). METHODS: This was a retrospective analysis of 41 patients who had MCSM with DCS treated with ACDF or LP from December 2018 to April 2023. Patients were split into ACDF and LP groups for comparison, and patients were further separated into subgroups based on whether or not a reserving canal space was present. The operation time, hemoglobin, hospital stay, modified Japanese Orthopaedic Association (mJOA) score, and visual analog scale (VAS) score were used to assess clinical efficacy. The C2-C7 Cobb angle, C2-C7 sagittal vertical axis, T1 slope, and cervical range of motion were applied to evaluate imaging changes. RESULTS: Of the 41 patients, 19 received ACDF, and 22 received LP. At the final follow-up, both groups' mJOA scores significantly improved, and the intercomparison showed no differences; the VAS score was much lower in the ACDF group but remained unchanged in the LP group. At the final follow-up, the C2-C7 Cobb angle and T1 slope had significantly increased in the ACDF group, while the LP group showed no change; the cervical range of motion had significantly decreased in both groups, with the ACDF group exhibiting a more marked reduction. Within the ACDF subgroup, there was no postoperative symptom improvement for those with reserving space, whereas there was postoperative symptom resolution for those with non-reserving space; however, postoperative symptom in the LP subgroup was resolved. CONCLUSIONS: Both ACDF and LP were efficacious for MCSM patients with DCS. While ACDF could improve cervical lordosis and alleviate neck pain more effectively, it can also result in cervical sagittal imbalance and decreased mobility. Furthermore, the recovery from LP was superior to that from ACDF for patients with reserving space. In contrast, the recovery from both decompression techniques was comparable for individuals in non-reserving space.

Predictive metabolomic signatures for safety assessment of three plastic nanoparticles using intestinal organoids.

Nanoplastic particles are pervasive environmental contaminants with potential health risks, while mouse intestinal organoids provide accurate in vitro models for studying these interactions. Metabolomics, especially through LC-MS, enables detailed cellular response studies, and there's a novel interest in comparing metabolic changes across nanoparticle species using gut organoids. This study used a mouse intestinal organoid combined with cell model to explore the differences in metabolites and toxicity mechanisms induced by exposure to three nanoplastics (PS, PTFE, and PMMA). The results showed that PS, PTFE, and PMMA exposure reduced mitochondrial membrane potential, intracellular ROS accumulation and oxidative stress, and inhibited the AKT/mTOR signaling pathway. Non-targeted metabolomics results confirmed that three types of nanoplastic particles regulate cellular status by regulating fatty acid metabolism, nucleotide metabolism, necroptosis and autophagy pathways. More importantly, these representative metabolites were further validated in model groups after mouse intestinal organoids and HCT116 cells were exposed to the respective NPs, indicating that organoid metabolomics results can be used to effectively predict toxicity. Untargeted metabolomics is sensitive enough to detect subtle metabolomic changes when functional cellular analysis shows no significant differences. Overall, our study reveals the underlying metabolic mechanism of NPs-induced intestinal organoid toxicity and provides new insights into the possible adverse consequences of NPs.

PG545 Prevents Osteoarthritis Development by Regulating PI3K/AKT/mTOR Signaling and Activating Chondrocyte Autophagy.

INTRODUCTION: Osteoarthritis (OA) is a degenerative disease common in the elderly and is characterized by joint pain, swelling, and restricted movement. In recent years, heparanase has been reported to play an important role in the development of osteoarthritic cartilage. PG545 is a heparan sulfate mimetic with heparanase inhibitory activity. In this study, the therapeutic effects and possible mechanisms of PG545 were investigated in a chondrocyte injury model induced by interleukin-1ß (IL -1ß). METHODS: Following treatment with PG545 or the autophagy inhibitor 3-methyladenine (3-MA), chondrocyte viability was detected using Cell Counting Kit-8 and fluorescein diacetate/propidium iodide double staining. The apoptosis rate of chondrocytes was determined by flow cytometry. Expression of light chain 3 and P62 was monitored by immunofluorescence labeling. Western blot, lentivirus infection with red fluorescent protein and green fluorescent protein, and quantitative real-time polymerase chain reaction were used to determine the expression levels of chondrocyte markers, apoptosis-related factors, autophagy proteins, and key proteins of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway. The expression and activity of stress-specific enzymes such as malondialdehyde, superoxide dismutase, and catalase (CAT) were investigated. Chondrocytes with ATG5 knockdown were used to investigate the relationship between the therapeutic effect of PG545 and autophagy. The therapeutic effect of PG545 was verified in vivo. RESULTS: PG545 had a significant protective effect on chondrocytes by reducing oxidative stress, apoptosis, and degradation of chondrocytes and increasing chondrocyte proliferation. PG545 was effective in inducing autophagy in IL-1ß-treated cells, while 3-MA attenuated the effect. The PI3K/Akt/mTOR pathway may be involved in the promotion of autophagy and OA treatment by PG545. CONCLUSION: PG545 was able to restore impaired autophagy and autophagic flux via the PI3K/Akt/mTOR pathway, thereby delaying the progression of OA, suggesting that PG545 may be a novel therapeutic approach for OA.

Long-term LDR exposure may induce cognitive impairments: A possible association through targeting gut microbiota-gut-brain axis.

Environmental and occupational low-dose radiation (LDR) exposure may be harmful for health but the previous reports regarding effect of LDR on cognition are contradictory. Here we investigated the effect of long-term LDR exposure on cognition. In this study, male Balb/c mice' cognitive functions were tested at 15 weeks after being exposed to 0.5 Gy LDR in 10 fractions at each dose of 0.05 Gy. The results demonstrated that long-term LDR exposure increases escape latency and the time spent in finding exits in mice compared with non LDR exposure. Meanwhile, the inflammation-related proteins including NFκB and p38 also increased. Lipopolysaccharide (LPS) increased and short-chain fatty acid (SCFA) levels decreased following long term LDR exposure. Treatment with microbiota-derived LPS and SCFAs reversed these effects in mice. Furthermore, the gut barrier integrity was damaged in a time-dependent manner with the decreased expression of intestinal epithelial-related biomarkers such as ZO-1 and occludin. Mechanistically, long after exposure to LDR, increased LPS levels may cause cognitive impairment through the regulation of Akt/mTOR signaling in the mouse hippocampus. These findings provide new insight into the clinical applications of LDR and suggest that the gut microbiota-plasma LPS and SCFAs-brain axis may underlie long-term LDR-induced cognition effects.

Low-dose radiation exaggerates HFD-induced metabolic dysfunction by gut microbiota through PA-PYCR1 axis.

Co-exposure of High-fat-diet (HFD) behavior and environmental low-dose radiation (LDR) is common among majority occupational workers, but the synergism of this co-exposure in metabolic health is poorly understood. This study aimed to investigate the impact of gut microbiota and its metabolites on the regulation of HFD accompanied by LDR-associated with metabolic dysfunction and insulin resistance. Here, we reported that Parasutterella was markedly elevated in the gut microbiota of mice in co-exposure of HFD and LDR, accompanied by increased pyrrolidinecarboxylic acid (PA) level in both intestine and plasma. Transplantation of fecal microbiota from mice with co-exposure HFD and LDR with metabolic dysfunction resulted in increased disruption of metabolic dysfunction, insulin resistance and increased PYCR1 (Pyrroline-5-carboxylate reductase 1) expression. Mechanistically, intestinal barrier was damaged more serious in mice with co-exposure of HFD and LDR, leading high PA level in plasma, activating PYCR1 expression to inhibit insulin Akt/mTOR (AKT kinase-transforming protein/Serine threonine-protein kinase) signaling pathway to aggravate HFD-induced metabolic impairments. This study suggests a new avenue for interventions against western diet companied with low dose radiation exposure-driven metabolic impairments.

Garlic oil alleviates high triglyceride levels in alcohol-exposed rats by inhibiting liver oxidative stress and regulating the intestinal barrier and intestinal flora.

Garlic oil (GO) is a kind of natural extract extracted from garlic, which has strong antioxidant activity. This study elucidates the protective mechanism of GO against alcohol-induced high triglyceride levels. Sixty male Sprague Dawley rats were assigned to five groups, including a control group (CON), a model group (MOD) treated with alcohol 56% v/v at 8 ml kg-1 day-1 for 2 weeks then 10 ml kg-1 day-1 for 8 weeks, a low-dose GO group (GO-L) given GO at 20 mg kg-1 day-1, a high-dose GO group (GO-H) given GO at 40 mg kg-1 day-1, and a positive group (POS) given diammonium glycyrrhizinate at 200 mg kg-1 day-1. The results showed that GO could significantly reduce the serum and liver triglyceride levels caused by alcohol exposure (p < .05). The GO-H group significantly reduced MDA level, increased SOD and GSH-Px levels in serum, liver, and colon (p < .05), significantly increased the levels of Sirt1 and PGC-1α proteins and reduced FoxO1 protein level in liver (p < .05), and significantly increased the levels of ZO-1 and Claudin1 proteins in the colon compared to the MOD group (p < .05). The 16S rRNA sequencing showed that the intestinal flora of the GO-H group was significantly changed compared with the MOD group. In summary, GO has the potential to improve high triglyceride levels in serum and liver induced by alcohol exposure, which may be related to the inhibition of oxidative stress regulation of Sirt1 and its downstream proteins, and to the restoration of the intestinal barrier and intestinal flora.

Tranexamic acid dosage for spinal surgery: a meta-analysis.

PURPOSE: We conducted this meta-analysis of randomized controlled trials (RCTs) to compare the efficacy of different doses of intravenous tranexamic acid (TXA) in spinal surgery. METHODS: We searched relevant academic articles from PubMed, Embase, the Cochrane Library, and CNKI. Two reviewers independently selected studies, assessed quality, extracted data, and evaluated the risk of bias. RevMan 5.4 was used for data analysis. RESULTS: Ten randomized controlled trials (RCTs) met the inclusion criteria and were identified, including 740 patients. According to the different dose regimens of intravenous TXA, the included studies' patients were divided into the high dose of intravenous TXA group and the low dose of intravenous TXA group. Compared with the low-dose group, the high-dose group can reduce the intraoperative blood loss (MD = - 100.87, 95% CI: [- 147.81, - 53.92], P < 0.0001). For the postoperative Hb and HCT, the high-dose group can separately maintain 4.54 g/dL (MD = 4.54, 95% CI: [2.08, 6.99], P = 0.003) and 1.27% (MD = 1.27, 95% CI: [0.59, 1.94], P = 0.0002). There were no statistically significant differences in total blood loss, preoperative Hb and HCT, operative time, and blood transfusion rate between the high-dose group and the low-dose group. CONCLUSIONS: Based on the present meta-analysis, compared with the low-dose of intravenous TXA in spinal surgery, the high dose of intravenous TXA decreases the intraoperative blood loss and preserves higher postoperative Hb and HCT levels without increasing the operative time and blood transfusion rate.

Antarctic krill oil ameliorates liver injury in rats exposed to alcohol by regulating bile acids metabolism and gut microbiota.

Bile acids (BAs) metabolism plays an important role in alcohol liver disease through the gut microflora-bile acids-liver axis. Antarctic Krill Oil (AKO) has protective effects on the liver, while whether AKO can protect against liver injury caused by alcohol is unclear. This study investigated the effects of AKO on BAs metabolism and intestinal microbiota in a rat model of alcohol-induced liver disease. Sprague-Dawley rats were randomly divided into five groups: control group, model group, low-dose AKO-treatment group (100 mg/kg/d), high-dose AKO-treatment group (200 mg/kg/d), and AKO control group (200 mg/kg/d). Administration of alcohol (8 to 10 mL/kg/d) for 16 weeks induced liver injury in rats. We found that AKO supplementation significantly protected the liver against alcohol-induced injury, evidenced by allayed hepatic histopathological changes, and inhibited the alcohol-induced elevation of serum biochemical indices. Furthermore, AKO could regulate BAs metabolism by activating the intestinal-hepatic FXR-FGF15-FGFR4 signaling axis with subsequently decreased cholesterol 7α-hydroxylase (CYP7A1) and sterol 12α-hydroxylase (CYP8B1) levels, reduced hepatic BAs production, decreased serum BAs level and increased fecal excretion of BAs. Additionally, 16S rDNA sequencing revealed that the gut microbiome richness and composition were altered in alcohol-treated rats in comparison to the control and AKO-administrated rats. Spearman's correlation analysis showed that differential gut bacterial genera correlated with the levels of BAs profiles in the serum, liver, and feces. These findings suggested that AKO dietary supplementation may protect against alcohol-induced liver injury through modulating BAs metabolism and altering the gut microbiome.

Folic acid intervention changes liver Foxp3 methylation and ameliorates the damage caused by Th17/Treg imbalance after long-term alcohol exposure.

Folic acid, as a key source of methyl donor in DNA methylation, has been proved to play a beneficial role in inflammation modulation, which is usually impaired in alcoholic liver disease (ALD). However, the role of folic acid in alcoholic liver inflammation and injury remain elusive. In this study, we sought to uncover the potential protective mechanism by which folic acid ameliorates alcoholic liver injury. 100 male C57BL/6J mice were randomly divided into 5 groups: normal saline group, folic acid control group (5 mg per kg BW), ethanol model group (56% v/v, 10 mL per kg BW), folic acid + ethanol group, and 5-Aza + ethanol group (0.1 mL per 20 g BW). Liquor (10 mL per kg BW) was orally administered 1 h after the folic acid treatment for 10 consecutive weeks. The results showed that folic acid-inhibited ethanol-induced serum TG, TC, and LDL elevation attenuated hepatic fat accumulation and maintained ALT at a normal level. 10 weeks of ethanol administration simultaneously upregulated the hepatic proportion of Th17 and Treg cells to different extents and broke the homeostasis of liver immunization. Folic acid limited ethanol-induced inflammatory injury by increasing the frequency of hepatic Treg cells. Importantly, this effect may be caused by decreased DNMT3a, which in turn downregulates the methylated levels of CPG2 and CPG3 in the Foxp3 promoter region, changing the abundance of Foxp3 expression and improving the Th17/Treg imbalance. In summary, our findings demonstrated that folic acid supplementation may relieve ethanol-induced Th17/Treg disbalance through altering Foxp3 promoter methylation patterns, suggesting that folic acid may be a feasible preventive strategy for ALD.

Potential role of PRKCSH in lung cancer: bioinformatics analysis and a case study of Nano ZnO.

PRKCSH, also known as glucosidase II beta, functions as a contributor to lung tumorigenesis by regulating the cell cycle in a p53-dependent manner under severe environmental stress. However, the prognostic value and molecular mechanisms by which the level of PRKCSH is significantly increased in cancer cells are not clearly understood. Here, we first generated a biological profile of PRKCSH expression changes in cancers by analysing bioinformatic data from cancer databases. We found that higher PRKCSH expression was correlated with a poorer prognosis and greater infiltration of most immune cell types in patients with lung cancer. In particular, PRKCSH expression showed significant negative correlations with the level of STAT6 (r = -0.31, p < 0.001) in lung cancer tissues. We further found that PRKCSH deficiency promoted G2/M arrest in response to zinc oxide nanoparticle (Nano ZnO) treatment in A549 cells. With regard to the mechanism, PRKCSH deficiency may induce STAT6 translocation to the nucleus to activate p53 expression through binding to the p53 promoter region from -365 bp to +126 bp. Eventually, activated p53 contributed to Nano-ZnO-induced G2/M arrest in lung cancer cells. Taken together, our data provide new insights into immunotherapy target choices and the prognostic value of PRKCSH. Since the G2/M cell cycle checkpoint is crucial for lung cancer prognosis, targeting PRKCSH expression to suppress the activation of the STAT6/p53 pathway is a potential therapeutic strategy for managing lung cancer.

Propolis Ameliorates Alcohol-Induced Depressive Symptoms in C57BL/6J Mice by Regulating Intestinal Mucosal Barrier Function and Inflammatory Reaction.

Accumulating evidence points to a critical role of the brain gut axis as an important paradigm for many central nervous system diseases. Recent studies suggest that propolis has obvious neuroprotective properties and functionality in regulating intestinal bacteria flora, hinting at a potential key effect at both terminals of this axis regulation. However, currently no clear evidence confirms the effects of propolis on alcohol-induced depression. Here, we establish an alcoholic depression model with C57BL/6J mice and demonstrate that treatment with propolis protects against alcohol-induced depressive symptoms by behavioral tests. In addition, propolis attenuates the injury of nerve cells in the hippocampal region and restores the serum levels of brain-derived neurotrophic factor (BDNF) and dopamine (DA) in mice with alcohol-induced depression. Pathology and biotin tracer assays show that propolis repairs the intestinal leakage caused by alcohol. Additionally, propolis treatment increases the expression levels of intestinal intercellular tight junctions' (TJs') structural proteins Claudin-1, Occludin and zona occludens-1 (ZO-1), as well as the activation state of the liver kinase B1/AMP-activated protein kinase (LKB1/AMPK) signaling pathway, which is closely related to the intestinal permeability. Furthermore, propolis can reduce the levels of pro-inflammatory, lipopolysaccharide (LPS) and fatty-acid-binding protein 2 (FABP2), suggesting the significance of the inflammatory response in alcoholic depression. Collectively, our findings indicate that propolis exerted an improving effect on alcohol-induced depressive symptoms by ameliorating brain gut dysfunction.

[Research progress of microRNA in laryngeal squamous cell carcinoma].

Laryngeal carcinoma is one of the most common malignant tumors in the area of head and neck, and the main pathological type is laryngeal squamous cell carcinoma. Due to the fact that the disease usually have no overt clinical symptoms at the early stage and easy to relapse, it has a poor prognosis and low five-year survival rate. microRNA is a class of endogenous, non-coding RNA with a length of 19-25 nucleotides. microRNAs, mainly regulate the expression of target genes at the post-transcriptional level after complementing and pairing with the 3'-UTR area of the target gene. Studies have shown that the abnormal expression of microRNA is closely related to the occurrence, development, metastasis and prognosis of various cancers including laryngeal carcinoma. In this article, the research progress of microRNA in laryngeal squamous cell carcinoma is reviewed.

[Research progress of cancer stem cell biomarkers in head and neck squamous cell carcinoma].

Cancer stem cells （CSCs）, as a few amount of tumors, have infinite replication, self-renewal, differentiation and regeneration of cell subsets with tumorigenicity, have close relationship with tumor occurrence and recurrence, which can be found in head and neck squamous cell carcinoma （HNSCC）. One of the important measures to improve the patient prognosis is monitoring cancer stem cells and timely clinical intervention. Biomarker detection of cancer stem cells is an important method for clinical monitoring of cancer stem cells. This article reviews the biomarkers of CSCs in HNSCC, which is consist of membrane surface markers, non-coding RNAs, target genes and proteins.

Inducing laccase activity in white rot fungi using copper ions and improving the efficiency of azo dye treatment with electricity generation using microbial fuel cells.

This work presents a white rot fungus-microbial fuel cell (WRF-MFC) that uses WRF that is grown at its cathode. Adding Cu2+ to the fungi-containing solid medium stimulated WRF-secreting laccase, which catalyzed the redox reaction in the MFC and thereby promoting the generation of electricity. Adding 12.5 mg L-1 Cu2+ to a G. lucidum-containing medium provided the greatest laccase stimulation and increased the laccase activity by a factor of 1.6. Adding 12.5 mg L-1 Cu2+ to the WRF chamber of WRF-MFC increased its decolorization of Acid Orange 7 (AO-7) and increased its power density to 223 mW m-2, which was 1.77 times that of an MFC without WRF. The enhancement of decolorization and electricity generation improved the performance of the WRF-MFC, indicating that a laccase-catalyzed cathode has great potential effectiveness in microbial fuel cells.

Vehicle emission and atmospheric pollution in China: problems, progress, and prospects.

China has been the largest vehicle market in the world since 2009. The stalemate between the rapid development of the vehicle industry and delayed vehicle emission control has become increasingly prominent. Vehicle emission has become a significant source of air pollution in China's cities. Understanding the current barriers in the vehicle industry is necessary for the development of effective and sustainable measures and policy to manage vehicle-induced air pollution. This review provides insight into the circumstances and causes of vehicle-induced air pollution and outlines recent progress in policy-makers' long-term strategies and regulations. The development of an integrated mechanism of social participation, technical revolution, and regulatory innovation in vehicles, fuel, and roads is suggested to break the stalemate between air pollution and the automobile boom in China; the implications of this review extend to other countries facing the similar atmospheric pollution problems.

MicroRNA485-3p negatively regulates the transcriptional co-repressor CtBP1 to control the oncogenic process in osteosarcoma cells.

Carboxyl-terminal binding protein 1 (CtBP1), a well-known transcriptional co-repressor, is highly expressed in a number of cancer types. However, it is still absent in osteosarcoma cells. Here, we found that CtBP1, but not CtBP2, is overexpressed in invasive osteosarcoma tissues and cells. The overexpressed CtBP1 in turn represses its downstream targets, such as the pro-apoptotic regulators Bax, Bim and p53 upregulated modulator of apoptosis (PUMA), cell adhesion molecule E-cadherin, and the cell cycle regulators p16, p21 and phosphatase and tensin homolog (PTEN). To explore the molecular mechanism of CtBP1 overexpression, we subjected three independent clinical samples to miRNA microarray analysis and found that miR-485-3p could specifically bind to the 3'-untranslated region (3'-UTR) of CtBP1, thereby negatively controlling CtBP1 expression. The overexpression of miR-485-3p in osteosarcoma cells significantly repressed CtBP1 levels and inhibited cell proliferation, colony formation, cell migration and sphere formation. Further analysis indicated that DNA hypermethylation in the promoter region of miR-485-3p caused the downregulation of miR-485-3p. Treatment with the DNA methylation inhibitor 5-aza-2'-deoxycytidine (AZA) resulted in the upregulation of miR-485-3p and the downregulation of CtBP1 as well as inhibited osteosarcoma cell growth. This study provides evidence that CtBP1 is also overexpressed in osteosarcoma cells and demonstrates the underlying mechanism regarding its overexpression. Thus, therapeutically targeting CtBP1 may represent an effective strategy for osteosarcoma therapy.