Near Full-Length Genome Characterization of Two Novel Unique Recombinants (CRF01_AE/CRF07_BC) in Beijing, China.

With the prevalence of human immunodeficiency virus type 1 (HIV-1) CRF01_AE and CRF07_BC subtypes in China, the co-circulation of multiple subtypes in the HIV-1-positive population may result in dual infection or superinfection in the population, leading to the emergence of unique recombinant forms (URFs) of the HIV-1 virus. In this study, two second-generation unique recombinant strains, BI0114 and BI0116, were identified, and their near full-length genome sequences were obtained. Recombination analysis showed that both sequences were isoforms of URF_0107, and they were second-generation unique recombinant strains formed by the recombination of CRF01_AE and CRF07_BC, with the isoforms being CRF01_AE and CRF0107_BC, respectively. The continued emergence of novel CRF01_AE/CRF07_BC recombinant strains suggests that the epidemiological, preventive, and control situation of HIV-1 is complex and that the relevant health authorities urgently need to establish responses to the challenges posed by changes in the pattern of strain recombination.

The Understanding and Compact Modeling of Reliability in Modern Metal-Oxide-Semiconductor Field-Effect Transistors: From Single-Mode to Mixed-Mode Mechanisms.

With the technological scaling of metal-oxide-semiconductor field-effect transistors (MOSFETs) and the scarcity of circuit design margins, the characteristics of device reliability have garnered widespread attention. Traditional single-mode reliability mechanisms and modeling are less sufficient to meet the demands of resilient circuit designs. Mixed-mode reliability mechanisms and modeling have become a focal point of future designs for reliability. This paper reviews the mechanisms and compact aging models of mixed-mode reliability. The mechanism and modeling method of mixed-mode reliability are discussed, including hot carrier degradation (HCD) with self-heating effect, mixed-mode aging of HCD and Bias Temperature Instability (BTI), off-state degradation (OSD), on-state time-dependent dielectric breakdown (TDDB), and metal electromigration (EM). The impact of alternating HCD-BTI stress conditions is also discussed. The results indicate that single-mode reliability analysis is insufficient for predicting the lifetime of advanced technology and circuits and provides guidance for future mixed-mode reliability analysis and modeling.

Increased prevalence and stable clustering rate of HIV-1 transmitted drug resistance strains after 'treat-all' in a megacity of China.

OBJECTIVES: The 'treat-all' strategy was implemented in Shenzhen, China in 2016. The effect of this extensive treatment on transmitted drug resistance (TDR) of HIV is unclear. METHODS: TDR analysis was performed, based on the partial HIV-1 pol gene obtained from the newly reported HIV-1 positive cases from 2011 to 2019 in Shenzhen, China. The HIV-1 molecular transmission networks were inferred to analyse the spread of TDR. Logistic regression was used to identify the potential risk factors with TDR mutations (TDRMs) to cluster. RESULTS: A total of 12 320 partial pol sequences were included in this study. The prevalence of TDR was 2.95% (363/12 320), which increased from 2.57% to 3.52% after 'treat-all'. The TDR prevalence was increased in populations with the characteristics of CRF07_BC, being single, educated to junior college level and above, MSM and male. The sensitivities of viruses to six antiretroviral drugs were decreased. The clustering rate of TDRMs remained stable, and the sequences in the three drug resistance transmission clusters (DRTCs) were mainly found during 2011-16. CRF07_BC and CRF55_01B were the factors associated with TDRMs clustering in the networks. CONCLUSIONS: The 'treat-all' strategy might have contributed to a small increase in TDR, while most of the TDRMs were distributed sporadically, which implies that the 'treat-all' strategy is helpful for the control of TDR in high-risk populations.

China's green data center development:Policies and carbon reduction technology path.

Data center is a very important infrastructure to support the development of information technology, and its development and increment are very remarkable. However, with the rapid and large-scale development of data centers, the problem of energy consumption turns to be also very prominent. Under the background of global carbon peak and carbon neutrality, developing green and low-carbon data centers has become an inevitable trend. This paper reviews and analyzes the policies and their roles in promoting China's green development of data centers in the past 10 years, summarizes the current situation of the implementation of green data center projects in China and gives the changes of PUE limits of data centers under the policy constraints. Application of green technologies is an important measure for energy-saving and low-carbon development of data centers, so encouraging innovation and application of green technologies in data center is also a priority task in relevant policies. This paper points out the green and low-carbon technology system of data centers, further summarizes energy-saving and carbon-reducing technologies in IT equipment, cooling system, power supply and distribution system, lighting, intelligent operation and maintenance, and provides an outlook on the future green development of data centers.

A Coupling Mechanism between Flicker Noise and Hot Carrier Degradations in FinFETs.

A coupling mechanism between flicker noise and hot carrier degradation (HCD) is revealed in this work. Predicting the flicker noise properties of fresh and aged devices is becoming essential for circuit designs, requiring an understanding of the fundamental noise behaviors. While certain models for fresh devices have been proposed, those for aged devices have not been reported yet because of the lack of a clear mechanism. The flicker noise of aged FinFETs is characterized based on the measure-stress-measure (MSM) method and analyzed from the device physics. It is found that both the mean and deviations of the noise power spectral density increase compared with the fresh counterparts. A coupling mechanism is proposed to explain the trap time constants, leading to the trap characterizations in their energy profiles. The amplitude and number of contributing traps are also changing and are dependent on the mode of HCD and determined by the position of the induced traps. A microscopic picture is developed from the perspective of trap coupling, reproducing well the measured noise of advanced nanoscale FinFETs. The finding is important for accurate flicker noise calculations and aging-aware circuit designs.

hucMSC-sEVs-Derived 14-3-3ζ Serves as a Bridge between YAP and Autophagy in Diabetic Kidney Disease.

As nanoscale membranous vesicles, human umbilical cord mesenchymal stem cell-derived small extracellular vesicles (hucMSC-sEVs) have attracted extensive attention in the field of tissue regeneration. Under the premise that the mechanisms of hucMSC-sEVs on the treatment of diabetic kidney disease (DKD) have not been revealed clearly, we constructed DKD rat model with success. After tail vein injection, hucMSC-sEVs effectively reduced blood glucose, maintained body weight and improved renal function in DKD rats. Notably, we found that hucMSC-sEVs suppressed YAP expression in renal cortical regions. Further in vitro experiments, we confirmed that the expression of YAP in the nucleus of renal podocytes was increased, and the level of autophagy was inhibited in the high-glucose environment, which could be reversed by intervention with hucMSC-sEVs. We screened out the key protein 14-3-3ζ, which could not only promote YAP cytoplasmic retention instead of entering the nucleus, but also enhance the level of autophagy in the cytoplasm. Ultimately, excessive YAP protein was removed by autophagy, a classic way of protein degradation. In conclusion, our study provides new strategies for the prevention of DKD and proposes the possibility of hucMSC-sEVs becoming a new treatment for DKD in the future.

Facet Engineering of a Metal-Organic Framework Support Modulates the Microenvironment of Palladium Nanoparticles for Selective Hydrogenation.

The exposed facets of supported catalysts play a crucial role in catalysis; however, they are usually ignored and related studies remain rare. Herein, we have fabricated a series of sandwich-structured metal-organic framework composites, denoted ZIF-8X @Pd@ZIF-8 (x represents the morphology of ZIF-8 core, i.e., ZIF-8C exposing (100) facet, ZIF-8RD exposing (110) facet, and ZIF-8TRD exposing mixed (100) and (110) facets), featuring Pd nanoparticles deposited on the specific crystal facets of ZIF-8 core, for hydrogenation of p-chloronitrobenzene. The Pd electronic state is tailored by the ZIF-8 core, where more electron-deficient Pd is found in ZIF-8C @Pd@ZIF-8 than that in ZIF-8RD @Pd@ZIF-8, leading to discriminative adsorption of the -NO2 and -Cl groups of p-chloronitrobenzene. Consequently, ZIF-8C @Pd@ZIF-8 exhibits excellent activity (97.6 %) and selectivity (98.1 %) to p-chloroaniline. This work highlights crystal facet engineering of supports to modulate the microenvironment and electronic state of supported metal nanoparticles, offering a promising avenue to enhanced catalysis.

Diagnostic and Therapeutic Roles of Extracellular Vesicles in Aging-Related Diseases.

Aging shows a decline in overall physical function, and cellular senescence is the powerful catalyst leading to aging. Considering that aging will be accompanied with the emergence of various aging-related diseases, research on new antiaging drugs is still valuable. Extracellular vesicles (EVs), as tools for intercellular communication, are important components of the senescence-associated secretory phenotype (SASP), and they can play pathological roles in the process of cellular senescence. In addition, EVs are similar to their original cells in functions. Therefore, EVs derived from pathological tissues or body fluids may be closely related to the progression of diseases and become potential biomarkers, while those from healthy cells may have therapeutic effects. Moreover, EVs are satisfactory drug carriers. At present, numerous studies have supported the idea that engineered EVs could improve drug targeting ability and utilization efficiency. Here, we summarize the characteristics of EVs and cellular senescence and focus on the diagnostic and therapeutic potential of EVs in various aging-related diseases, including Alzheimer disease, osteoporosis, cardiovascular disease, diabetes mellitus and its complications, and skin aging.

Neutrophil membrane engineered HucMSC sEVs alleviate cisplatin-induced AKI by enhancing cellular uptake and targeting.

Human umbilical cord mesenchymal stem cells-derived small extracellular vesicles (hucMSC-sEVs) have been demonstrated as a therapeutic agent to prevent and treat cisplatin-induced acute kidney injury (AKI). However, hucMSC-sEVs still face many problems and challenges in the repair and treatment of tissue injury, including short circulation time, insufficient targeting, and low therapeutic efficacy. Therefore, we constructed engineered hybrid vesicles fused with nanovesicles derived from human neutrophil membranes and hucMSC-sEVs, named neutrophil membrane engineered hucMSC-sEVs (NEX). NEX significantly enhanced the targeting of hucMSC-sEVs to injured kidney tissues, improved the impaired renal function via reducing pro-inflammatory cytokines expression, promoted the proliferation of renal tissue cells, and inhibited renal cell apoptosis in vivo. In addition, NEX enhanced hucMSC-sEVs uptake by NRK52E cells, but inhibited its uptake by RAW264.7 cells. Moreover, administration of NEX reduced cellular oxidative stress and promoted proliferation of NRK52E cells treated with cisplatin in vitro. In summary, our findings indicate that this design of a universal approach enhances the targeting and therapeutic efficacy of hucMSC-sEVs in kidney tissue regeneration, and provides new evidence promoting its clinical application.

Optimizing Pt Electronic States through Formation of a Schottky Junction on Non-reducible Metal-Organic Frameworks for Enhanced Photocatalysis.

Charge transfer between metal sites and supports is crucial for catalysis. Redox-inert supports are usually unfavorable due to their less electronic interaction with metal sites, which, we demonstrate, is not always correct. Herein, three metal-organic frameworks (MOFs) are chosen to mimic inert or active supports for Pt nanoparticles (NPs) and the photocatalysis is studied. Results demonstrate the formation of a Schottky junction between Pt and the MOFs, leading to the electron-donation effect of the MOFs. Under light irradiation, both the MOF electron-donation effect and Pt interband excitation dominate the Pt electron density. Compared with the "active" UiO-66 and MIL-125 supports, Pt NPs on the "inert" ZIF-8 exhibit higher electron density due to the higher Schottky barrier, resulting in superior photocatalytic activity. This work optimizes metal catalysts with non-reducible supports, and promotes the understanding of the relationship between the metal-support interaction and photocatalysis.

MSC-Derived Extracellular Vesicle-Delivered L-PGDS Inhibit Gastric Cancer Progression by Suppressing Cancer Cell Stemness and STAT3 Phosphorylation.

Mesenchymal stem cell- (MSC-) derived extracellular vesicles (EVs) serving as delivery system have attracted extensive research interest, especially in cancer therapy. In our previous study, lipocalin-type prostaglandin D2 synthase (L-PGDS) showed inhibitory effects on gastric cancer growth. In this study, we aimed to explore whether MSC-EV-delivered L-PGDS (EVs-L-PGDS) could inhibit gastric cancer progression. EVs-L-PGDS were generated from MSCs transfected with adenovirus encoding L-PGDS. Cell colony-forming, migration, invasion, and flow cytometry assays were used to show the inhibitory effects of EVs on tumor cells in vitro, and the nude mouse subcutaneous tumor model was performed to show the inhibitory effect of EVs on tumor progression in vivo. In vitro, EVs-L-PGDS could be internalized and inhibit the colony-forming, migration, and invasion ability of gastric cancer cell SGC-7901 and promote cell apoptosis. In vivo, EVs-L-PGDS inhibited the tumor growth in nude mouse subcutaneous tumor-bearing model. Compared with the PBS and EVs containing empty vector (EVs-Vector) group, more apoptotic cells and higher L-PGDS expression were detected in tumor tissue of the EVs-L-PGDS treatment group. And these differences are significant. Mechanistically, EVs-L-PGDS reduced the expression of stem cell markers including Oct4, Nanog, and Sox2 and inhibited STAT3 phosphorylation in gastric cancer cell SGC-7901. In conclusion, our results imply that MSC-derived EVs could be utilized as an effective nanovehicle to deliver L-PGDS for gastric cancer treatment, which provides a novel idea for the EV-based cancer therapy.

The construction and application of a blended teaching model under the strategic background of healthy China.

In order to cultivate the ability of independent learning and lifelong learning of medical students, improve the ability of students to analyze and solve problems, improve the competence of medical talents and cultivate high-level and innovative talents, we have constructed the blended teaching model of "Clinical Case Investigation-Online Open Course Learning-Classroom PBL Seminar-After-Class Health Education". At the same time, an ability-oriented performance evaluation system improved the teaching quality feedback system has also established. This article introduces the construction and application of the blended teaching model, as well as the problems it faces, provides a theoretical basis for the optimization and improvement of this model. It also provides a model theory and practical basis for creating a blended online and offline "golden course" for the professional courses of medical laboratory technology.

Roles of Mesenchymal Stem Cell-Derived Exosomes in Cancer Development and Targeted Therapy.

Exosomes have emerged as a new drug delivery system. In particular, exosomes derived from mesenchymal stem cells (MSCs) have been extensively studied because of their tumor-homing ability and yield advantages. Considering that MSC-derived exosomes are a double-edged sword in the development, metastasis, and invasion of tumors, engineered exosomes have broad potential use. In this review, we focused on the latest development in the treatment of tumors using engineered and nonengineered MSC-derived exosomes (MSC-EXs). Nonengineered MSC-EXs exert an antitumor effect on several well-studied tumors by affecting tumor growth, angiogenesis, metastasis, and invasion. Furthermore, engineered exosomes have promising research prospects as drug-carrying tools for the transport of miRNAs, small-molecule drugs, and proteins. Although exosomes lack uniform standards in terms of definition, separation, and purification, they still have great research value because of their unique advantages, such as high biocompatibility and low toxicity. Future studies on MSC-EXs should elucidate the mechanisms underlying their anticancer effect and the safety of their application.

Platelet-rich plasma promotes MSCs exosomes paracrine to repair acute kidney injury via AKT/Rab27 pathway.

Acute kidney injury (AKI) is defined by rapid deterioration of renal function, and is a common complication in hospitalized patients. Among the recent therapeutic options, mesenchymal stem cells (MSCs) are considered a promising therapeutic strategy for damaged tissue repair. Platelet rich plasma (PRP) regulates mesenchymal cells to repair tissue damage through the release of growth factors. In this study, we proposed a possible therapeutic use of MSCs stimulated by platelet-rich plasma (PRP-MSCs) in a glycerin-induced AKI murine model. In vivo and in vitro studies, showed that PRP-MSCs could significantly attenuate serum blood urea nitrogen and creatinine levels, and reverse the histopathological kidney damage. PRP-MSCs treatment reduced renal tubular cell apoptosis stimulated by glycerin. We confirmed that PRP promoted the proliferation and reinforced the stemness of MSCs by inducing YAP nucleus expression, and that PRP promoted MSCs exosomes in a paracrine manner to repair AKI through an activated AKT/Rab27 pathway. Our results revealed that the PRP stimulated MSCs paracrine pathway could effectively alleviate glycerin-induced AKI. Therefore, PRP pretreatment may be a new method to improve the therapeutic effect of MSCs.

HucMSC exosome-delivered 14-3-3ζ alleviates ultraviolet radiation-induced photodamage via SIRT1 pathway modulation.

Exosomes derived from human umbilical cord mesenchymal stem cells (hucMSC-ex) are nano-sized membrane-bound vesicles that have been reported to facilitate skin regeneration and repair. However, the roles played by hucMSC-ex in ultraviolet (UV) radiation-induced skin photodamage and the underlying mechanisms remain unknown. To investigate the functions of hucMSC-ex in a rat model of acute skin photodamage, immunofluorescence and immunohistochemical staining, quantitative real-time-polymerase chain reaction (qRT-PCR), western blot, and gene silencing assays were performed. We found that the in vivo subcutaneous injection of hucMSC-ex elicited antioxidant and anti-inflammatory effects against UV radiation-induced DNA damage and apoptosis. Further studies showed that the sirtuin 1 (SIRT1) expression level in skin keratinocytes (HaCaT) decreased in a time- and dose-dependent manner under in vitro UV radiation induced-oxidative stress conditions, which could be reversed by treatment with hucMSC-ex. The activation of SIRT1 significantly attenuated UV- and H2O2-induced cytotoxic damage by inhibiting oxidative stress and promoting the activation of autophagy. Our study found that 14-3-3ζ protein, which was delivered by hucMSC-ex, exerted a cytoprotective function via the modulation of a SIRT1-dependent antioxidant pathway. Collectively, our findings indicated that hucMSC-ex might represent a new potential agent for preventing or treating UV radiation-induced skin photodamage and aging.

Circular RNA ITCH suppresses metastasis of gastric cancer via regulating miR-199a-5p/Klotho axis.

Circular RNAs (circRNAs) are considered as a new regulatory factor in growth, metastasis and therapeutic resistance of human cancers. But the clinical significance and underlying mechanism of circular RNA ITCH (circ-ITCH) in gastric cancer (GC) remain unknown. In the present study, we found that circ-ITCH was down-regulated in GC cell lines, GC tissues and their serum-derived exosomes. The level of circ-ITCH was related to invasion depth. Functional assays showed that circ-ITCH overexpression inhibited the proliferation, migration, invasion and epithelial mesenchymal transition (EMT) of GC cells, whereas circ-ITCH knockdown appeared an opposite effect. Bioinformatic analysis and luciferase reporter assay confirmed that circ-ITCH acted as miR-199a-5p sponge and increased the level of Klotho. The expression level of miR-199-5p was up-regulated in GC tissues and negatively correlated with that of circ-ITCH. MiR-199a-5p mimics reversed the effects on inhibiting metastasis induced by circ-ITCH overexpression and decreased the level of Klotho in GC cells. Our findings indicate that circ-ITCH suppresses metastasis of GC by acting as the sponge of miR-199a-5p and increasing Klotho expression, which serves as a potential biomarker and targets for the diagnosis and therapy of GC.Abbreviations: CircRNAs: circular RNAs; GC: gastric cancer; circ-ITCH: circular RNA Itchy E3 ubiquitin protein ligase; ceRNA: competitive endogenous RNA; EMT: Epithelial-mesenchymal transition; siRNA: Small interfering RNA; TEM: transmission electron microscope; NTA: nanoparticle tracking analysis.

Exosomes Derived from Human Umbilical Cord Mesenchymal Stem Cells Accelerate Cutaneous Wound Healing by Enhancing Angiogenesis through Delivering Angiopoietin-2.

The underlying mechanisms of human umbilical cord mesenchymal stem cells (hucMSCs) and their exosomes (hucMSC-Exs), which play significant roles in skin wound healing, remain poorly understood. By using a rat model of deep second-degree burn injury, the roles of hucMSC-Exs in angiogenesis and cutaneous wound healing in vivo were investigated. We found that hucMSC-Exs accelerated skin wound healing and angiogenesis, inducing a higher wound-closure rate and increased expression of CD31 in vivo. We also discovered that hucMSC-Exs contained angiopoietin-2 (Ang-2), and treatment with hucMSC-Exs enhanced the expression of the Ang-2 protein in the wound area and human umbilical vein endothelial cells (HUVECs) through exosomal-mediated Ang-2 transfer. Moreover, hucMSC-Exs promoted the proliferative, migratory, and tube-forming ability of HUVECs. Furthermore, overexpression of Ang-2 in hucMSC-Exs further enhanced HUVEC migration and tube formation and exerted therapeutic and proangiogenic effects in cutaneous wounds in rats, whereas knockdown of Ang-2 in hucMSC-Exs abrogated these therapeutic and proangiogenic effects. Taken together, our results indicated that hucMSC-Ex-derived Ang-2 plays a significant role in tube formation of HUVECs and promotion of angiogenesis, and further suggested that hucMSC-Ex-based therapy may serve as a promising therapeutic approach for promoting cutaneous wound healing.

Gastric-cancer-derived mesenchymal stem cells: a promising target for resveratrol in the suppression of gastric cancer metastasis.

The tumor microenvironment (TM) is an essential factor of tumor progression. Mesenchymal stem cells (MSCs) are important components of the TM and play critical roles in cancer metastasis. Resveratrol (RES) is a potential antitumor drug that has attracted extensive attention. However, it remains unclear whether RES can exert its antitumor activity by targeting MSCs located in the TM. In this study, we demonstrated that the conditioned medium of gastric-cancer-derived MSCs (GC-MSCs) promoted gastric cancer (GC) metastasis and facilitated the progression of epithelialmesenchymal transition (EMT) of GC cells. However, after pretreatment with RES, the prometastatic effect of GC-MSCs on GC cells was reversed. Furthermore, RES reduced GC-MSC (IL-6, IL-8, MCP-1, VEGF) gene expression and protein secretion, and counteracted the activation of the GC-MSC-induced Wnt/ß-catenin signaling of GC cells, with less ß-catenin nuclear transport and declined expression of ß-catenin, CD44, and CyclinD3 in GC cells. Re-expression of ß-catenin impaired the inhibitory effect of RES on GC cells. In conclusion, RES restricted the mobility increase of GC cells and reversed the progress of EMT induced by GC-MSCs by inactivating the Wnt/ß-catenin signaling. GC-MSCs are promising target for RES in the inhibition of GC metastasis.

The role and mechanism of miR-374 regulating the malignant transformation of mesenchymal stem cells.

MicroRNAs (miRNAs) play important roles in cell transformation and carcinogenesis. We have previously established a tumor cell line K3 transformed from rat bone marrow-derived mesenchymal stem cells (rBM-MSCs). However, the underlying mechanism involved in MSC transformation remains unclear. Herein, we identified the key miRNAs that regulate the transformation of rBM-MSCs, and clarified their biological roles. Microarray and qRT-PCR results showed an increased expression of miR-374 but decreased expressions of miR-199a, miR-145, miR-34a, and miR-214 in K3 cells compared to rBM-MSCs. MiR-374 overexpression in rBM-MSCs increased the colony number and the proportion of the cells in S-phase. In addition, miR-374 overexpression reduced E-cadherin expression and increased N-cadherin expression in rBM-MSCs, promoting the migration ability of these cells. On the contrary, miR-374 knockdown in K3 cells led to impaired proliferation and migration capacities. Furthermore, wnt5a was identified as a target gene of miR-374. MiR-374 overexpression upregulated ß-catenin expression in rBM-MSCs while miR-374 knockdown downregulated that in K3 cells. In conclusion, miR-374 promotes the proliferation and migration of transformed MSCs by regulating Wnt5a/ß-catenin signaling pathway, which provides evidence for the contribution of miRNA to MSC transformation and suggests a new role of miR-374 in cancer development and progression.

Exosomal TRIM3 is a novel marker and therapy target for gastric cancer.

BACKGROUND: Exosomes are critically involved in cancer development and progression. The exosomal contents have been suggested as ideal cancer biomarkers. In this study, we investigated the expression of exosomal proteins in the serum of gastric cancer patients and their roles in gastric cancer. METHODS: The proteomic profile of exosomes from the serum of gastric cancer patients was detected by using LC-MS/MS. The expression of TRIM3 in exosomes from the serum of gastric cancer patients and healthy controls was assessed by ELISA and western blot. Immunohistochemistry was used to detect TRIM3 expression in gastric cancer tissues and their matching adjacent tissues. The growth and migration abilities of gastric cancer cells with TRIM3 overexpression or knockdown in vitro were evaluated by colony formation assay and transwell migration assay. The effects of TRIM3 overexpression or knockdown on gastric cancer growth and metastasis in vivo were investigated by using subcutaneous xenograft tumor and peritoneal metastasis mouse model. The effects of TRIM3-overexpressing exosomes on gastric cancer growth and metastasis in vitro and in vivo were also evaluated. RESULTS: We found that the expression levels of TRIM3 mRNA and protein were decreased in gastric cancer tissues compared to the matched control tissues. In addition, the levels of TRIM3 protein in the serum exosomes of gastric cancer patients were lower than that in healthy controls. We demonstrated that TRIM3 overexpression reduced while TRIM3 knockdown promoted the growth and metastasis of gastric cancer in vitro and in vivo through the regulation of stem cell factors and EMT regulators. Moreover, exosomes-mediated delivery of TRIM3 protein could suppress gastric cancer growth and metastasis in vitro and in vivo. CONCLUSIONS: Taken together, our findings suggest that exosomal TRIM3 may serve as a biomarker for gastric cancer diagnosis and the delivery of TRIM3 by exosomes may provide a new avenue for gastric cancer therapy.