INTRODUCTION:Proteomics research provides significant insights for the diagnosis and treatment of diseases. Protein ratios reflect biological connections between related proteins and can help identify clinically relevant loci. Exploring the relationship between plasma protein-to-protein ratios and aneurysms may help identify new targets for prevention and treatment. METHODS:We performed a two-sample Mendelian Randomization (MR) analysis to assess the associations between 2,821 protein ratios and various types of aneurysms. Twostep MR was utilized to investigate the potential mediating role of cardiometabolic factors. Through pathway enrichment analysis and drug target evaluation, we further elucidated the potential mechanisms and therapeutic targets related to aneurysms. RESULTS:After MR analysis, we identified 12 protein ratios with significant causal associations with aneurysms. Among them, seven protein ratios were associated with Thoracic Aortic Aneurysms (TAA), three with Aortic Aneurysms (AA), one with Abdominal Aortic Aneurysms (AAA), and one with Subarachnoid Hemorrhage (SAH). No significant causal associations were identified for unruptured intracranial aneurysm. We further performed a two-step MR analysis and found associations between cardiometabolic traits like blood pressure and lipids with aneurysms, confirming their potential mediating roles between protein ratios and aneurysms. Lastly, our drug target evaluation suggested that anti-inflammatory and lipid-lowering drugs are associated with aneurysm-related protein ratios. DISCUSSION:We identified 12 plasma protein ratios significantly associated with aneurysms, with blood pressure and lipids potentially mediating these associations. Additionally, our findings suggest that anti-inflammatory and lipid-lowering drugs are associated with the 12 plasma protein ratios, offering new insights for the treatment of aneurysms. CONCLUSIONS:Our findings elucidate the significant associations between 12 plasma protein ratios and aneurysms. These results provide new perspectives for the prevention and management of aneurysms.

Myocardial apoptosis is a cardinal process in acute viral myocarditis (VMC) instigated by coxsackievirus B3 (CVB3) infection. The anti-apoptotic regulator protein deglycase DJ-1 (DJ-1) is implicated in several pathological processes, yet its role in CVB3-induced VMC remains obscure. In this study, we decipher the protective role of DJ-1 against VMC. We found decreased DJ-1 expression in CVB3-infected H9C2 cells and VMC mouse heart tissues. DJ-1 knockout exacerbated VMC severity and apoptosis. Conversely, recovery of DJ-1 levels showed protective effects in vitro and in vivo. We observed downregulation of Dusp1 in DJ-1-deficient mice hearts and H9C2 cells with DJ-1 silencing. Subsequent in vitro assays corroborated that downregulation of DJ-1 amplifies apoptosis in H9C2 cells following CVB3 infection. This effect is mediated through the suppression of Dusp1 expression, thereby triggering the activation of the P38MAPK signaling pathway. Overall, our findings underscore DJ-1 as an appealing therapeutic target for VMC, with its anti-apoptotic effects in CVB3-induced VMC mediated in part via the Dusp1/P38MAPK signaling pathway. This novel understanding of DJ-1's regulation might provide fresh insights into the pathogenesis of VMC and a potential therapeutic avenue for VMC.

Hernia typically does not heal spontaneously. Large-pore patches, most notably polypropylene patches (PP patches), are the gold standard in hernia repair surgery. However, a single patch is insufficient for both anti-adhesion and tissue fusion, leading to complications such as organ adhesions. In this study, a chemically stable and biocompatible modified fluorinated poly(aryl ether) (FPAE-F) was prepared by grafting perfluoroalkyl groups onto a fluorinated poly(aryl ether) via nucleophilic aromatic substitution. A porous FPAE-F fiber film (eFPAE-F) was fabricated by electrospinning and combined with a PP patch to produce a modified fluorinated poly(aryl ether)/polypropylene (FPAE-F/PP) composite patch. The eFPAE-F layer of the composite patch, which faces the abdominal viscera, exhibits a water contact angle of 151.3 ± 1.2°. This superhydrophobic surface prevents protein adhesion, thereby inhibiting rapid fibroblast proliferation. The small pore size (3.22 ± 1.25 μm) of the eFPAE-F layer effectively impedes fibroblast infiltration while permitting the transport and metabolism of nutrients. In vivo experiments have demonstrated that the composite patch is a viable anti-adhesion material, resulting in no adhesions and low inflammation levels after 2 weeks. Due to its outstanding anti-adhesion properties, eFPAE-F/PP is expected to be applied in the field of hernia repair.

Imbalance of proinflammatory and anti-inflammatory responses plays a crucial role in the progression of abdominal aortic aneurysms. ILF3, a known modulator of the innate immune response, is involved in cardiovascular diseases. This study aims to investigate the role of ILF3 in abdominal aortic aneurysm formation. Here, we use multi-omics analyzes, transgenic male mice, and multiplex immunohistochemistry to unravel the underlying involvement of ILF3 in abdominal aortic aneurysms. The results show that macrophage ILF3 deficiency attenuates abdominal aortic aneurysm progression, while elevated macrophage ILF3 exacerbates abdominal aortic aneurysm lesions. Mechanistically, we reveal that macrophagic ILF3 increases NF-κB activity by hastening the decay of p105 mRNA, leading to amplified inflammation in macrophages. Meanwhile, ILF3 represses the anti-inflammatory action by inhibiting the Keap1-Nrf2 signaling pathway through facilitating the ILF3/eIF4A1 complex-mediated enhancement of Keap1 translational efficiency. Moreover, Bardoxolone Methyl treatment alleviates the severity of abdominal aortic aneurysm lesions in the context of elevated ILF3 expression. Together, our findings underscore the significance of macrophage ILF3 in abdominal aortic aneurysm development and suggest its potential as a promising therapeutic target for abdominal aortic aneurysms. Here the authors investigate the involvement of the immune modulator ILF3 in abdominal aortic aneurysm, showing that macrophage ILF3 promotes aneurysm progression by increasing NF-kB activity and inhibiting Keap1-Nrf2 signaling.

Hyperglycemia accelerates calcification of atherosclerotic plaques in diabetic patients, and the accumulation of advanced glycation end products (AGEs) is closely related to the atherosclerotic calcification. Here, we show that hyperglycemia-mediated AGEs markedly increase vascular smooth muscle cells (VSMCs) NF90/110 activation in male diabetic patients with atherosclerotic calcified samples. VSMC-specific NF90/110 knockout in male mice decreases obviously AGEs-induced atherosclerotic calcification, along with the inhibitions of VSMC phenotypic changes to osteoblast-like cells, apoptosis, and matrix vesicle release. Mechanistically, AGEs increase the activity of NF90, which then enhances ubiquitination and degradation of AGE receptor 1 (AGER1) by stabilizing the mRNA of E3 ubiquitin ligase FBXW7, thus causing the accumulation of more AGEs and atherosclerotic calcification. Collectively, our study demonstrates the effects of VSMC NF90 in mediating the metabolic imbalance of AGEs to accelerate diabetic atherosclerotic calcification. Therefore, inhibition of VSMC NF90 may be a potential therapeutic target for diabetic atherosclerotic calcification. The accumulation of AGEs is closely related to the atherosclerotic calcification in diabetic patients. Here, the authors find that VSMC NF90 knockout attenuates diabetic atherosclerotic calcification by mediating the metabolic imbalance of AGEs.

Heart failure (HF) remains prevalent in patients who survived myocardial infarction (MI). Despite the accessibility of the primary percutaneous coronary intervention and medications that alleviate ventricular remodeling with functional improvement, there is an urgent need for clinicians and basic scientists to further reveal the mechanisms behind post-MI HF as well as investigate earlier and more efficient treatment after MI. Growing numbers of studies have highlighted the crucial role of macrophages in cardiac repair and remodeling following MI, and timely intervention targeting the immune response via macrophages may represent a promising therapeutic avenue. Recently, technology such as single-cell sequencing has provided us with an updated and in-depth understanding of the role of macrophages in MI. Meanwhile, the development of biomaterials has made it possible for macrophage-targeted therapy. Thus, an overall and thorough understanding of the role of macrophages in post-MI HF and the current development status of macrophage-based therapy will assist in the further study and development of macrophage-targeted treatment for post-infarction cardiac remodeling. This review synthesizes the spatiotemporal dynamics, function, mechanism and signaling of macrophages in the process of HF after MI, as well as discusses the emerging bio-materials and possible therapeutic agents targeting macrophages for post-MI HF.

The objective of this research is to clarify the impact of periodontitis on overall and cardiovascular-related death rates among hypertensive individuals. A total of 5665 individuals with hypertension were included from the National Health and Nutrition Examination Survey (NHANES) data spanning 2001–2004 and 2009–2014. These individuals were divided into two groups based on the presence or absence of periodontitis and further stratified by the severity of periodontitis. We employed weighted multivariate Cox proportional hazards regression and Kaplan-Meier curves (log-rank test) to evaluate the impact of periodontitis on all-cause and cardiovascular mortality. Additional analyses, including adjustments for various covariates, subgroups, and sensitivity analyses, were conducted to ensure the robustness and reliability of our results. Over an average follow-up duration of 10.22 years, there were 1,122 all-cause and 297 cardiovascular deaths. Individuals with periodontitis exhibited an elevated risk of all-cause mortality (HR = 1.33, 95

We describe a microwave-assisted, methanol and acetic acid-free, inexpensive method for rapid staining of SDS-PAGE proteins. Only citric acid, benzoic acid, and Coomassie brilliant blue G-250 (CBG) were used. Microwave irradiation reduced the detection duration, and proteins in a clear background were visualized within 30 min of destaining, after 2 min of fixing and 12 min of staining. By using this protocol, comparable band intensities were obtained to the conventional methanol/acetic acid method.

Diabetes mellitus significantly escalates the risk of accelerated atherosclerosis (AS), severely affecting cardiovascular health. Our research, leveraging Gene Expression Omnibus (GEO) database analysis (GSE118481), revealed diminished TFPI2 expression in diabetic patients' atherosclerotic plaques. Further validation in carotid artery plaques and an AS mouse model confirmed TFPI2's reduced expression in diabetes. Through TFPI2 knockdown in non-diabetic mice, we observed aggravated plaque burden and increased inflammatory M1 macrophage polarization. Conversely, TFPI2 overexpression in diabetic mice improved plaque stability and induced reparative M2 macrophage polarization, countering hyperglycemia's negative effects. Mechanistically, transcription factor activator protein 2α (AP-2α) is a repressor of PPPARg transcription, and the interaction of TFPI2 with the transcription factor AP-2α blocks AP-2α binding to the PPARγ gene promoter, which is essential for PPARγ-mediated transcription and the transition from M1 to M2 macrophages. Additionally, hyperglycemia-induced DNA methyltransferase 1 (DNMT1) upregulation heightens TFPI2 methylation, reducing its expression. Our findings spotlight the TFPI2/AP-2α/PPARγ axis as crucial in diabetic AS modulation, proposing its targeting as a new therapeutic strategy to halt diabetes-driven AS progression, highlighting TFPI2's therapeutic promise in addressing diabetes-related cardiovascular issues.

Recently, the supra-normal left ventricular ejection fraction (snLVEF) has been proposed, based on extensive datasets indicating increased all-cause mortality in individuals with an LVEF exceeding 65%. However, the implications of an LVEF > 65% in the context of acute coronary syndrome (ACS) remain underexplored.The aim of the present study was to investigate the correlation between supra-normal left ventricular ejection fraction (snLVEF) and major adverse cardiovascular events (MACE) in patients with ACS.Methods: A total of 874 ACS patients (560 men, mean age 59.5 ± 10.0; 314 women, mean age 61.5 ± 8.9) who underwent their first coronary angiography during the period from March 2013 to October 2015 were divided into 2 groups: normal LVEF (nLVEF) (55% ≤ EF ≤ 65%) and snLVEF (EF > 65%), according to their echocardiography results. The patients were evaluated for MACE after surgery by collecting clinical data and long-term follow-up data. This correlation was further analyzed by Kaplan-Meier analysis and Cox regression analysis.The follow-up data revealed a significantly higher incidence of MACE among snLVEF patients compared to the nLVEF group (15.6% versus 7.4%; P = 0.020). This heightened risk persisted even after adjustment for multiple variables, indicating a strong association between snLVEF and increased MACE risk (HR: 2.346; 95% CI: 1.196-4.602; P = 0.013).SnLVEF was independently associated with poor prognosis after ACS. Enhanced management strategies for snLVEF patients could potentially reduce the incidence of MACE in ACS patients.

BACKGROUND:This study aimed to investigate the relationship of dyslipidemia and interleukin-enhancer binding factor 3 (ILF3) in gastric cancer, and provide insights into the potential application of statins as an agent to prevent and treat gastric cancer.METHODS:The expression levels of ILF3 in gastric cancer were examined with publicly available datasets such as TCGA, and western blotting and immunohistochemistry were performed to determine the expression of ILF3 in clinical specimens. The effects of ox-LDL on expression of ILF3 were further verified with western blot analyses. RNA sequencing, Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Ontology (GO), and Gene Set Enrichment Analysis (GSEA) pathway analyses were performed to reveal the potential downstream signaling pathway targets of ILF3. The effects of statins and ILF3 on PI3K/AKT/mTOR signaling pathway, cell proliferation, cell cycle, migration and invasion of gastric cancer cells were investigated with Edu assay, flow cytometry and transwell assay.RESULTS:Immunohistochemistry and western blot demonstrated that the positive expression rates of ILF3 in gastric cancer tissues were higher than adjacent mucosa tissues. The ox-LDL promoted the expression of ILF3 in a time-concentration-dependent manner. ILF3 promoted the proliferation, cell cycle, migration and invasion by activating the PI3K/AKT/mTOR signaling pathway. Statins inhibited the proliferation, cell cycle, migration and invasion of gastric cancer by inhibiting the expression of ILF3.CONCLUSIONS:These findings demonstrate that ox-LDL promotes ILF3 overexpression to regulate gastric cancer progression by activating the PI3K/AKT/mTOR signaling pathway. Statins inhibits the expression of ILF3, which might be a new targeted therapy for gastric cancer.

Background:Salvianolic acid B (Sal B) is a representative component of phenolic acids derived from the dried root and rhizome of Salvia miltiorrhiza Bge. (Labiatae), which promotes angiogenesis in myocardial infarction and diabetic cardiomyopathy. However, whether Sal B has a neuroprotective function in ischemic stroke by promoting angiogenesis is still unclear.Methods:In the present study, ischemic stroke models were induced in rats by middle cerebral artery occlusion (MCAO), and Sal B (10 or 20 mg/kg/d) was intraperitoneally injected according to a previous study. Neurological deficits were evaluated by the modified Longa five-point scale, modified Bederson scores and cerebral infarction sizes by triphenyltetrazolium chloride (TTC) staining. Apoptotic cells were tested by cleaved-caspase3 immunofluorescence staining and an in situ cell death (TUNEL) detection kit. Human umbilical vein endothelial cells (HUVECs) exposed to hypoxia were used to investigate the effects of Sal B on angiogenesis and tube formation in vitro.Results:Sal B ameliorated the neurological deficits, decreased the cerebral infarction volumes in rats with ischemic stroke, significantly increased the expression of vascular endothelial growth factor receptor 2 (VEGFR2) and VEGFA and promoted angiogenesis both in vivo and in vitro. Furthermore, Sal B increased stanniocalcin 1 (STC1) expression, induced the phosphorylation of protein kinase B (AKT) and mammalian target of rapamycin (mTOR) activity, enhanced cell migration, and activated VEGFR2/VEGFA signaling in endothelial cells.Conclusions:This study showed that Sal B promoted angiogenesis and alleviated neurological apoptosis in rats with ischemic stroke by promoting STC1.

Diabetes mellitus (DM) promotes neointimal hyperplasia, characterized by dysregulated proliferation and accumulation of vascular smooth muscle cells (VSMCs), leading to occlusive disorders, such as atherosclerosis and stenosis. Poly (ADP-ribose) polymerase 1 (PARP1), reported as a crucial mediator in tumor proliferation and transformation, has a pivotal role in DM. Nonetheless, the function and potential mechanism of PARP1 in diabetic neointimal hyperplasia remain unclear. In this study, we constructed PARP1 conventional knockout (PARP1-/-) mice, and ligation of the left common carotid artery was performed to induce neointimal hyperplasia in Type I diabetes mellitus (T1DM) mouse models. PARP1 expression in the aorta arteries of T1DM mice increased significantly and genetic deletion of PARP1 showed an inhibitory effect on the neointimal hyperplasia. Furthermore, our results revealed that PARP1 enhanced diabetic neointimal hyperplasia via downregulating tissue factor pathway inhibitor (TFPI2), a suppressor of vascular smooth muscle cell proliferation and migration, in which PARP1 acts as a negative transcription factor augmenting TFPI2 promoter DNA methylation. In conclusion, these results suggested that PARP1 accelerates the process of hyperglycemia-induced neointimal hyperplasia via promoting VSMCs proliferation and migration in a TFPI2 dependent manner.

Protein deglycase DJ‐1 (DJ‐1) is a multifunctional protein involved in various biological processes. However, it is unclear whether DJ‐1 influences atherosclerosis development and plaque stability. Accordingly, we evaluated the influence of DJ‐1 deletion on the progression of atherosclerosis and elucidate the underlying mechanisms. We examine the expression of DJ‐1 in atherosclerotic plaques of human and mouse models which showed that DJ‐1 expression was significantly decreased in human plaques compared with that in healthy vessels. Consistent with this, the DJ‐1 levels were persistently reduced in atherosclerotic lesions of ApoE−/− mice with the increasing time fed by western diet. Furthermore, exposure of vascular smooth muscle cells (VSMCs) to oxidized low‐density lipoprotein down‐regulated DJ‐1 in vitro. The canonical markers of plaque stability and VSMC phenotypes were evaluated in vivo and in vitro. DJ‐1 deficiency in Apoe−/− mice promoted the progression of atherosclerosis and exaggerated plaque instability. Moreover, isolated VSMCs from Apoe−/−DJ‐1−/− mice showed lower expression of contractile markers (α‐smooth muscle actin and calponin) and higher expression of synthetic indicators (osteopontin, vimentin and tropoelastin) and Kruppel‐like factor 4 (KLF4) by comparison with Apoe−/−DJ‐1+/+ mice. Furthermore, genetic inhibition of KLF4 counteracted the adverse effects of DJ‐1 deletion. Therefore, our results showed that DJ‐1 deletion caused phenotype switching of VSMCs and exacerbated atherosclerotic plaque instability in a KLF4‐dependent manner.

Background Early-onset scoliosis (EOS), defined by an onset age of scoliosis less than 10 years, conveys significant health risk to affected children. Identification of the molecular aetiology underlying patients with EOS could provide valuable information for both clinical management and prenatal screening. Methods In this study, we consecutively recruited a cohort of 447 Chinese patients with operative EOS. We performed exome sequencing (ES) screening on these individuals and their available family members (totaling 670 subjects). Another cohort of 13 patients with idiopathic early-onset scoliosis (IEOS) from the USA who underwent ES was also recruited. Results After ES data processing and variant interpretation, we detected molecular diagnostic variants in 92 out of 447 (20.6%) Chinese patients with EOS, including 8 patients with molecular confirmation of their clinical diagnosis and 84 patients with molecular diagnoses of previously unrecognised diseases underlying scoliosis. One out of 13 patients with IEOS from the US cohort was molecularly diagnosed. The age at presentation, the number of organ systems involved and the Cobb angle were the three top features predictive of a molecular diagnosis. Conclusion ES enabled the molecular diagnosis/classification of patients with EOS. Specific clinical features/feature pairs are able to indicate the likelihood of gaining a molecular diagnosis through ES.

Calcification is common in atherosclerotic plaque and can induce vulnerability, which further leads to myocardial infarction, plaque rupture and stroke. The mechanisms of atherosclerotic calcification are poorly characterized. Interleukin enhancer binding factor 3 (ILF3) has been identified as a novel factor affecting dyslipidemia and stroke subtypes. However, the precise role of ILF3 in atherosclerotic calcification remains unclear. In this study, we used smooth muscle-conditional ILF3 knockout (ILF3SM-KO) and transgenic mice (ILF3SM-Tg) and macrophage-conditional ILF3 knockout (ILF3M-KO) and transgenic (ILF3M-Tg) mice respectively. Here we showed that ILF3 expression is increased in calcified human aortic vascular smooth muscle cells (HAVSMCs) and calcified atherosclerotic plaque in humans and mice. We then found that hyperlipidemia increases ILF3 expression and exacerbates calcification of VSMCs and macrophages by regulating bone morphogenetic protein 2 (BMP2) and signal transducer and activator of transcription 1 (STAT1) transcription. We further explored the molecular mechanisms of ILF3 in atherosclerotic calcification and revealed that ILF3 acts on the promoter regions of BMP2 and STAT1 and mediates BMP2 upregulation and STAT1 downregulation, which promotes atherosclerotic calcification. Our results demonstrate the effect of ILF3 in atherosclerotic calcification. Inhibition of ILF3 may be a useful therapy for preventing and even reversing atherosclerotic calcification.

Background: Adenocarcinoma of the esophagogastric junction (AEG) refers to cancer that crosses the line of the gastroesophageal junction and includes distal esophageal cancer and proximal gastric cancer. It is characterized by early metastasis and a poor prognosis and has few treatment options. Here, we report a novel potential therapeutic target, hematological and neurological expressed 1-like (HN1L), in AEG. Methods: A total of 38 patients who underwent surgical resection of AEG at the Department of Thoracic Surgery of Shandong Provincial Hospital from September 2018 to June 2019 were enrolled into the study. We detected the expression of HN1L in AEG and adjacent nontumor tissues by IHC staining. The clinicopathological characteristics of HN1L were statistically analyzed. Then, the expression of HN1L in different cell lines was detected by RT-q PCR. Finally, AGS and HGC-27 cell lines were performed to inhibit HN1L by shRNA in order to explore its role in the development of AEG. Results: Immunohistochemical staining showed that the expression of HN1L in cancer tissues was higher than that in nontumor tissue (p < 0.001). High expression of HN1L was significantly correlated with TNM stage (p = 0.013) and lymph node metastasis (p = 0.03). The expression of HN1L was upregulated in tumor cell lines compared with normal cell line. Additionally, Cell function studies demonstrated that lentivirus-mediated shRNA silencing of HN1L expression could effectively reduce the proliferation, invasion, and metastasis of tumor cell lines and promote their apoptosis (p < 0.05). Conclusions: HN1L expression might contribute to the invasion and metastasis of AEG and is a promising therapeutic target.

BACKGROUND:Salvianolic acid B (Sal B) is the representative component of phenolic acids derived from the dried root and rhizome of Salvia miltiorrhiza Bge. (Labiatae), which has been widely used for the treatment of cardiovascular and cerebrovascular diseases. However, the effect of Sal B on diabetic cardiomyopathy (DCM) is still unclear.METHODS:Type 1 diabetes mellitus was induced in C57BL/6 J mice by streptozotocin (STZ) treatment, whereas meanwhile Salvianolic Acid B (Sal B (15 or 30 mg/kg/d) was intraperitoneally injected for 16 weeks. At the end of this period, cardiac function was assessed by echocardiography, and total collagen deposition was evaluated by Masson's trichrome and Picrosirius Red staining. Human umbilical vein endothelial cells exposed to hypoxia were used to investigate the effect of different doses of Sal B on angiogenesis and tube formation in vitro. Transcriptome sequencing was performed to identify potential targets of Sal B.RESULTS:Sal B ameliorated left ventricular dysfunction and remodeling, and decreased collagen deposition in the heart of diabetic mice. Administration of Sal B increased the expression of vascular endothelial growth factor (VEGF) receptor 2 (VEGFR2) and VEGFA in a dose-dependent manner and promoted angiogenesis both in vivo and in vitro. Furthermore, Sal B reduced HG-induced insulin-like growth factor-binding protein 3 (IGFBP3) expression, induced the phosphorylation of extracellular signal-regulated protein kinase and protein kinase B (AKT) activities, enhanced cell proliferation, and activated VEGFR2/VEGFA signaling in endothelial cells. The underlying mechanisms involve SalB that enhances IGFBP3 promoter DNA methylation and induce nuclear translocation of IGFBP3 in HUVECs under hypoxia.CONCLUSIONS:Sal B promoted angiogenesis and alleviated cardiac fibrosis and cardiac remodeling in DCM by suppressing IGFBP3.

Gastric cancer (GC) is lethal and there is an urgent need for improved understanding of this disease. Recent studies have reported that microRNAs (miRNAs) play increasingly important roles in the regulation of GC. In this study, we explored the target genes and effects of miR-7641 in GC. Our data showed that high miR-7641 expression was associated with low expression of ARID1A in GC tissue. miR-7641 expression promoted GC cell proliferation and colony formation. Luciferase reporter assay results confirmed that ARID1A was a target gene of miR-7641. Furthermore, downregulation of ARID1A expression caused a significant increase in GC cell proliferation. In vivo depletion of miR-7641 reduced tumor volume and weight and increased ARID1A and Ki67 expression as well as a decreased terminal-deoxynucleotidyl transferase-mediated nick end labeling in mouse tumor tissues. Conversely, ARID1A silencing reversed the suppressive effects of miR-7641 inhibitors on GC cells. Overall, these findings indicate that miR-7641 is a promising novel prognostic biomarker of GC and may represent a novel target for clinical management of GC.