The mammalian actin elongation factor ENAH/MENA contributes to autophagosome formation via its actin regulatory function.

Macroautophagy/autophagy is a catabolic process crucial for degrading cytosolic components and damaged organelles to maintain cellular homeostasis, enabling cells to survive in extreme extracellular environments. ENAH/MENA, a member of the Ena/VASP protein family, functions as a highly efficient actin elongation factor. In this study, our objective was to explore the role of ENAH in the autophagy process. Initially, we demonstrated that depleting ENAH in cancer cells inhibits autophagosome formation. Subsequently, we observed ENAH's colocalization with MAP1LC3/LC3 during tumor cell starvation, dependent on actin cytoskeleton polymerization and the interaction between ENAH and BECN1 (beclin 1). Additionally, mammalian ATG9A formed a ring-like structure around ENAH-LC3 puncta during starvation, relying on actin cytoskeleton polymerization. Furthermore, ENAH's EVH1 and EVH2 domains were found to be indispensable for its colocalization with LC3 and BECN1, while the PRD domain played a crucial role in the formation of the ATG9A ring. Finally, our study revealed ENAH-led actin comet tails in autophagosome trafficking. In conclusion, our findings provide initial insights into the regulatory role of the mammalian actin elongation factor ENAH in autophagy.

Construction of a Two-Dimensional GO/Ti3C2TX Composite Membrane and Investigation of Mg2+/Li+ Separation Performance.

Graphene oxide (GO) two-dimensional (2D) membranes with unique layer structures and tunable layer spacing have special advantages and great potential in the field of water treatment. However, GO membranes face the issues of weak anti-swelling ability as well as poor permeability. We prepared GO/Ti3C2TX 2D composite membranes with 2D/2D structures by intercalating Ti3C2TX nanosheets with slightly smaller sizes into GO membranes. Ti3C2TX intercalation can effectively expand the layer spacing of GO, thereby substantially enhancing the flux of the composite membrane (2.82 to 6.35 L·m-2·h-1). Moreover, the GO/Ti3C2TX composite membrane exhibited a good Mg2+/Li+ separation capability. For the simulated brine, the separation factor of M2 was 3.81, and the salt solution flux was as high as 5.26 L·m-2·h-1. Meanwhile, the incorporation of Ti3C2TX nanosheets significantly improved the stability of GO/Ti3C2TX membranes in different pH environments. This study provides a unique insight into the preparation of highly permeable and ion-selective GO membranes.

Ba3(BS3)(PS4): the first alkaline-earth metal thioborate-thiophosphate with strong optical anisotropy originating from planar [BS3] units.

The first alkaline-earth metal thioborate-thiophosphate Ba3(BS3)(PS4) was designed from Ba3(BO3)(PO4) by S-O substitution and fabricated experimentally. The [BS3] pseudo-layers formed in the structure contribute to the strong optical anisotropy and a large birefringence of ∼0.11 at 1064 nm. The results enrich the structural and chemical diversity of chalcogenides.

Research on the Antibacterial Properties of MXene-Based 2D-2D Composite Materials Membrane.

Novel MXene-based two-dimensional (2D) membranes are widely used for water purification due to their highly controllable structure and antibacterial properties. However, in the process of membrane separation, the problems of membrane fouling, especially biological fouling, limits the further application of MXene-based membranes. In this study, in order to improve the antibacterial and separation properties of membranes, three kinds of MXene-based 2D-2D composite membranes (M2~M4) were prepared using polyethersulfone (PES) as the substrate, which were GO@MXene, O-g-C3N4@MXene and BiOCl@MXene composite membranes respectively. The results showed that the antibacterial activity of M2~M4 against Escherichia coli and Staphylococcus aureus was further improved, especially the antibacterial ratio of M4 against Escherichia coli and Staphylococcus aureus was up to 50% and 82.4%, respectively. By comparing the surface morphology of MXene membrane and modified membrane treated bacteria through scanning electron microscopy (SEM), it was found that the cell density on modified membrane was significantly lower than that of pure MXene membrane.

Zn2 HgP2 S8 : A Wide Bandgap Hg-Based Infrared Nonlinear Optical Material with Large Second-Harmonic Generation Response.

Hg-based chalcogenides, as good candidates for the exploration of high-performance infrared (IR) nonlinear optical (NLO) materials, usually exhibit strong NLO effects, but narrow bandgaps. Herein, an unprecedented wide bandgap Hg-based IR NLO material Zn2 HgP2 S8 (ZHPS) with diamond-like structure is rationally designed and fabricated by a tetrahedron re-organization strategy with the aid of structure and property predictions. ZHPS exhibits a wide bandgap of 3.37 eV, which is the largest one among the reported Hg-based chalcogenide IR NLO materials and first breaks the 3.0 eV bandgap "wall" in this system, resulting in a high laser-induced damage threshold (LIDT) of ≈2.2 × AgGaS2 (AGS). Meanwhile, it shows a large NLO response (1.1 × AGS), achieving a good balance between bandgap (≥3.0 eV) and NLO effect (≥1 × AGS) for an excellent IR NLO material. DFT calculations uncover that, compared to normal [HgS4 ]n , highly distorted [HgS4 ]d tetrahedral units are conducive to generating wide bandgap, and the wide bandgap in ZHPS can be attributed to the strong s-p hybridization between Hg─S bonding in distorted [HgS4 ]d , which gives some insights into the design of Hg-based chalcogenides with excellent properties based on distorted [HgS4 ]d tetrahedra.

NF kappa B regulator Bcl3 controls development and function of classical dendritic cells required for resistance to Toxoplasma gondii.

The atypical IκB family member Bcl3 associates with p50/NF-κB1 or p52/NF-κB2 homodimers in the nucleus, and positively or negatively modulates transcription in a context-dependent manner. In mice lacking Bcl3 globally or specifically in CD11c+ cells, we previously reported that Toxoplasma gondii infection is uniformly fatal and is associated with an impaired Th1 immune response. Since Bcl3 expression in dendritic cells (DC) is pivotal for antigen presentation and since classical DCs (cDC) are major antigen presenting cells, we investigated the role of Bcl3 specifically in cDCs in vivo by crossing Zbtb46 cre mice with Bcl3flx/flx mice. Bcl3flx/flx Zbtb46 cre mice were as susceptible to lethal T. gondii infection as total Bcl3-/- mice and generated poor Th1 immune responses. Consistent with this, compared to wildtype controls, splenic Xcr1+ Bcl3-deficient cDC1 cells were defective in presenting Ova antigen to OT-I cells both for Ova257-264 peptide and after infection with Ovalbumin-expressing T. gondii. Moreover, splenic CD4+ and CD8+ T cells from infected Bcl3flx/flx Zbtb46 cre mice exhibited decreased T. gondii-specific priming as revealed by both reduced cytokine production and reduced T. gondii-specific tetramer staining. In vitro differentiation of cDCs from bone marrow progenitors also revealed Bcl3-dependent cDC-specific antigen-presentation activity. Consistent with this, splenocyte single cell RNA seq (scRNAseq) in infected mice revealed Bcl3-dependent expression of genes involved in antigen processing in cDCs. We also identified by scRNAseq, a unique Bcl3-dependent hybrid subpopulation of Zbtb46+ DCs co-expressing the monocyte/macrophage transcription factor Lysozyme M. This subpopulation exhibited Bcl3-dependent expansion after infection. Likewise, by flow cytometry we identified two T. gondii-induced hybrid subpopulations of Bcl3-dependent cDC1 and cDC2 cells both expressing monocyte/macrophage markers, designated as icDC1 and icDC2. Together, our results indicate that Bcl3 in classical DCs is a major determinant of protective T cell responses and survival in T. gondii-infection.

Reticulon 2 promotes gastric cancer metastasis via activating endoplasmic reticulum Ca2+ efflux-mediated ERK signalling.

Gastric cancer ranks fourth for mortality globally among various malignant tumours, and invasion and metastasis are the major reason leading to its poor prognosis. Recently, accumulating studies revealed the role of reticulon proteins in cell growth and transmigration. However, the expression and biological function of reticulon proteins in human gastric cancer remain largely unclear. Herein, we explored the potential role of reticulon 2 (RTN2) in the progression of gastric cancer. Tissue microarray was used to determine the expression levels of RTN2 in 267 gastric cancer patients by immunohistochemistry. Gastric cancer cell lines were utilised to examine the influences of RTN2 on cellular migration and invasion abilities, epithelial-to-mesenchymal transition (EMT) and signalling pathway. In vivo studies were also performed to detect the effect of RTN2 on tumour metastasis. We found that RTN2 expression was notably upregulated in tumour tissues compared to pericarcinomatous tissues. High RTN2 expression was positively correlated with patients' age, vessel invasion, tumour invasion depth, lymph node metastasis and TNM stage. Besides, high RTN2 staining intensity was associated with adverse survival which was further identified as an independent prognostic factor for gastric cancer patients by multivariate analysis. And the predictive accuracy was also improved when incorporated RTN2 into the TNM-staging system. RTN2 could promote the proliferation, migration and invasion of gastric cancer cells in vitro and lung metastasis in vivo. Mechanistically, RTN2 interacted with IP3R, and activated ERK signalling pathway via facilitating Ca2+ release from the endoplasmic reticulum, and subsequently drove EMT in gastric cancer cells. These results proposed RTN2 as a novel promotor and potential molecular target for gastric cancer therapies.

Tumor size and perineural invasion predict outcome of gastric high-grade neuroendocrine neoplasms.

A new subcategory, grade 3 neuroendocrine tumors, is incorporated into the grading system of pancreatic neuroendocrine neoplasms in the 2017 WHO classification in order to differentiate grade 3 neuroendocrine tumors from neuroendocrine carcinomas. The 2019 WHO classification extends the concept of grade 3 neuroendocrine tumors to gastrointestinal high-grade neuroendocrine neoplasms. However, there is still limited study focusing on the gastric grade 3 neuroendocrine tumors and gastric neuroendocrine carcinomas. We retrospectively enrolled 151 gastric high-grade neuroendocrine neoplasms patients, who underwent radical resection from January 2007 to December 2015. Clinicopathologic and prognostic features were studied. The Surveillance, Epidemiology, and End Results (SEER) database was used to verify the prognostic determinants found in the Zhongshan cohort. Neuroendocrine carcinomas showed a higher Ki67 index and higher mitotic count than grade 3 neuroendocrine tumors. We identified 109 (72.2%) patients with neuroendocrine carcinomas, 12 (7.9%) patients with grade 3 neuroendocrine tumors, and 30 (19.9%) patients with mixed neuroendocrine-non-neuroendocrine neoplasms. Although neuroendocrine carcinomas demonstrated higher Ki67 index (P = 0.004) and mitoses (P = 0.001) than grade 3 neuroendocrine tumors, their prognosis after radical resection did not demonstrate significant differences (P = 0.709). Tumor size, perineural invasion, and TNM stage were independent prognostic factors of gastric high-grade neuroendocrine neoplasms.

Bcl-3 suppresses differentiation of RORγt+ regulatory T cells.

Regulatory T cells (Tregs) exert inhibitory function under various physiological conditions and adopt diverse characteristics following environmental cues. Multiple subsets of Tregs expressing master transcription factors of helper T cells such as RORγt, T-bet, Gata3 and PPARγ have been characterized, but the molecular mechanism governing the differentiation of these subsets remains largely unknown. Here we report that the atypical IκB protein family member Bcl-3 suppresses RORγt+ Treg accumulation. The suppressive effect of Bcl-3 was particularly evident in the mouse immune tolerance model of anti-CD3 therapy. Using conditional knockout mice, we illustrate that loss of Bcl-3 specifically in Tregs was sufficient to boost RORγt+ Treg formation and resistance of mice to dextran sulfate sodium-induced colitis. We further demonstrate the suppressive effect of Bcl-3 on RORγt+ Treg differentiation in vitro. Our results reveal a novel role of nuclear factor-kappa B signaling pathways in Treg subset differentiation that may have clinical implications in immunotherapy.

The NF-κB regulator Bcl-3 restricts terminal differentiation and promotes memory cell formation of CD8+ T cells during viral infection.

Bcl-3 is an atypical member of the IκB family that acts in the nucleus to modulate transcription of many NF-κB targets in a highly context-dependent manner. Accordingly, complete Bcl-3-/- mice have diverse defects in both innate and adaptive immune responses; however, direct effects of Bcl-3 action in individual immune cell types have not been clearly defined. Here, we document a cell-autonomous role for Bcl-3 in CD8+ T cell differentiation during the response to lymphocytic choriomeningitis virus infection. Single-cell RNA-seq and flow cytometric analysis of virus-specific Bcl3-/- CD8+ T cells revealed that differentiation was skewed towards terminal effector cells at the expense of memory precursor effector cells (MPECs). Accordingly, Bcl3-/- CD8+ T cells exhibited reduced memory cell formation and a defective recall response. Conversely, Bcl-3-overexpression in transgenic CD8+ T cells enhanced MPEC formation but reduced effector cell differentiation. Together, our results establish Bcl-3 as an autonomous determinant of memory/terminal effector cell balance during CD8+ T cell differentiation in response to acute viral infection. Our results provide proof-of-principle for targeting Bcl-3 pharmacologically to optimize adaptive immune responses to infectious agents, cancer cells, vaccines and other stimuli that induce CD8+ T cell differentiation.

Bcl-3 inhibits lupus-like phenotypes in BL6/lpr mice.

Bcl-3 is an atypical member of the IκB family that modulates NF-κB activity in nuclei. lpr mice carry the lpr mutation in Fas, resulting in functional loss of this death receptor; they serve as models for lupus erythematosus and autoimmune lymphoproliferation syndrome (ALPS). To explore the biologic roles of Bcl-3 in this disease model, we generated BL6/lpr mice lacking Bcl-3. Unlike lpr mice on an MRL background, BL6/lpr mice present with very mild lupus- or ALPS-like phenotypes. Bcl-3 KO BL6/lpr mice, however, developed severe splenomegaly, dramatically increased numbers of double negative T cells - a hallmark of human lupus, ALPS, and MRL/lpr mice - and exhibited inflammation in multiple organs, despite low levels of autoantibodies, similar to those in BL6/lpr mice. Loss of Bcl-3 specifically in T cells exacerbated select lupus-like phenotypes, specifically organ infiltration. Mechanistically, elevated levels of Tnfα in Bcl-3 KO BL6/lpr mice may promote lupus-like phenotypes, since loss of Tnfα in these mice reversed the pathology due to loss of Bcl-3. Contrary to the inhibitory functions of Bcl-3 revealed here, this regulator has also been shown to promote inflammation in different settings. Our findings highlight the profound, yet highly context-dependent roles of Bcl-3 in the development of inflammation-associated pathology.

High intratumoral expression of eIF4A1 promotes epithelial-to-mesenchymal transition and predicts unfavorable prognosis in gastric cancer.

Gastric cancer is an important health problem, being the fifth most common cancer and the third leading cause of cancer-related death worldwide. Aberrant protein translation contributes to the oncogenesis and development of cancers, and upregulation of translation initiation factor eIF4A1 has been observed in several kinds of malignancies. However, the role of eIF4A1 in gastric cancer progression remains unclear. In this study, we found that the expression of eIF4A1, a component of translation initiation complex, was increased in gastric cancer. High expression of eIF4A1 was positively associated with poor tumor differentiation, late T stage, lymph node metastasis, advanced TNM stage, and poor prognosis in patients with gastric cancer. Overexpression of eIF4A1 promoted the migration and invasion of gastric cancer cells in vitro and enhanced tumor metastasis in nude mice model. Mechanism studies revealed that eIF4A1 induced epithelial-to-mesenchymal transition (EMT) of gastric cancer cells through driving the translation of SNAI1 mRNA. Together, these findings indicate that eIF4A1 promotes EMT and metastasis of gastric cancer and suggest that eIF4A1 is a potential target for the adjuvant therapy for gastric cancer patients.

Hormonal Suppression of Stem Cells Inhibits Symmetric Cell Division and Gastric Tumorigenesis.

Cancer is believed to arise from stem cells, but mechanisms that limit the acquisition of mutations and tumor development have not been well defined. We show that a +4 stem cell (SC) in the gastric antrum, marked by expression of Cck2r (a GPCR) and Delta-like ligand 1 (DLL1), is a label-retaining cell that undergoes predominant asymmetric cell division. This +4 antral SC is Notch1low/ Numb+ and repressed by signaling from gastrin-expressing endocrine (G) cells. Chemical carcinogenesis of the stomach is associated with loss of G cells, increased symmetric stem cell division, glandular fission, and more rapid stem cell lineage tracing, a process that can be suppressed by exogenous gastrin treatment. This hormonal suppression is associated with a marked reduction in gastric cancer mutational load, as revealed by exomic sequencing. Taken together, our results show that gastric tumorigenesis is associated with increased symmetric cell division that facilitates mutation and is suppressed by GPCR signaling.

IL-20-Receptor Signaling Delimits IL-17 Production in Psoriatic Inflammation.

IL-17 cytokines, in particular IL-17A, are critical effectors in psoriasis. Antibodies that block IL-17A are highly efficacious in treating psoriasis. Likewise, disruption of IL-17 cytokines signaling, such as via the loss of the adaptor CIKS/Act1, ameliorates inflammation in mouse models of psoriasis. IL-17A promotes a cascade of effects, including the robust production of IL-19 in both humans and mice. IL-19, along with IL-20 and IL-24, signal via IL-20 receptors and comprise a subgroup within the IL-10 cytokine family. The role of these three cytokines in psoriasis is unresolved. They have been linked to inflammatory processes, including psoriatic pathology, but these cytokines have also been reported to suppress inflammation in other contexts. In this study, we demonstrate that signaling via IL-20 receptors, including in response to IL-19, delimited aspects of imiquimod-induced psoriatic inflammation. IL-20 receptor signaling suppressed the dermal production of the CCL2 chemokine and thereby reduced CCL-2-driven infiltration of inflammatory cells into the dermis, including IL-17A-producing γδT cells. This constitutes a negative feedback, since IL-17A strongly induces IL-19 in keratinocytes. The effects of IL-17 cytokines in this inflammatory setting are dynamic; they are central to the development of both dermal and epidermal hallmarks of psoriasis but also initiate a path to mitigate inflammatory damage.

IL-25 Orchestrates Activation of Th Cells via Conventional Dendritic Cells in Tissue to Exacerbate Chronic House Dust Mite-Induced Asthma Pathology.

House dust mite (HDM) extract is a common trigger of asthma in humans. Chronic exposure to HDM also induces asthma-like pathology in mice. Allergic responses to HDM and other allergens are linked to release of IL-25, IL-33, and TSLP by epithelial cells; these cytokines, especially IL-33, target innate lymphoid cells type 2 to produce type 2 cytokines. To what extent and by what mechanisms IL-25 contributes to chronic HDM-induced pathology is not well understood. In humans, elevated levels of IL-25 appear to be associated with cases of uncontrolled asthma and exacerbated attacks. In this article, we demonstrate that blockade of IL-25 signaling in either lung conventional dendritic cells or in T cells resulted in similar decreases in production of IL-13 and IL-9 by T cells, reduced mast cell accumulation and tissue remodeling, and improved lung function but had only modest effects on eosinophilia. Stimulation of conventional dendritic cells by IL-25 promoted proximal accumulation of Th cells, and stimulation of Th cells by IL-25 locally promoted IL-13 and IL-9 production. IL-25 made notable contributions to chronic HDM-induced allergic asthma pathology by facilitating clustering and cross-stimulation of different cell types in tissue. Therapeutic targeting of IL-25 in combination with other treatments may be beneficial.

Histamine H1 type receptor antagonist loratadine ameliorates oxidized LDL induced endothelial dysfunction.

Oxidized LDL (ox-LDL) is one of the major risk factors of atherosclerosis. Endothelial dysfunction caused by ox-LDL is an early event in the pathogenesis of cardiovascular diseases. Preclinical studies have been performed to explore efficient means of preventing endothelial abnormalities. In this study, we revealed that loratadine, a histamine H1 type receptor specific antagonist, possesses a protective effect by relieving ox-LDL-induced endothelial inflammation. Treatment of endothelial cells with ox-LDL induces expression of the H1 receptor. The presence of loratadine in endothelial culture efficiently suppressed ox-LDL-induced attachment of monocytes to endothelial cells, production of ROS and vascular adhesion molecules, and induction cytokines including VCAM-1, E-selectin, TNF-α, IL-6 and IL-8. Mechanistically, we show that loratadine potently blocks ox-LDL-induced JNK activation as well as the AP-1 and NF-κB signaling pathways. Collectively, our data disclose a new role for loratadine in endothelial protection.

Mannan-oligosaccharide modulates the obesity and gut microbiota in high-fat diet-fed mice.

The gut microbiota is considered to be associated with high-fat diet (HFD)-induced obesity and metabolic syndrome (MS). Mannan-oligosaccharide (MOS) is widely used as a natural additive, and its effect on promoting fat metabolism has been reported. Here, we performed a 11-week study on C57BL/6J mice fed a high-fat diet (HFD) with/without MOS supplementation, and the results showed that MOS could attenuate high-fat diet induced metabolic syndrome, including slower body weight gain, lowered serum lipids and reduced insulin resistance. Next generation sequencing (NGS) of the gut microbiota indicated that MOS modulated the overall structure of the gut microbiome, which was highly correlated with MS parameters. Specifically, the intake of MOS decreased the Firmicutes/Bacteroidetes ratio and could reverse the changes in the relative abundance of several species caused by HFD, including Akkermansia muciniphila, Bacteroides acidifaciens, Lactobacillus gasseri and Bifidobacterium pseudolongum. Thus, MOS has the potential to be used as a new prebiotic for regulating the gut microbiota and helping in attenuating metabolic disorders.

High expression of tumor necrosis factor receptor-associated factor 2 promotes tumor metastasis and is associated with unfavorable prognosis in gastric cancer.

BACKGROUND: Tumor necrosis factor receptor-associated factor 2 (TRAF2) is a key effector in the activation of nuclear factor kappa B (NF-κB). Nevertheless, the role of TRAF2 in gastric tumorigenesis remains little defined. METHODS: Immunohistochemistry was used to find the relationship between TRAF2 expression and clinicopathological characteristics of gastric cancer patients, and nomogram was applied to predict the overall survival of patients. Besides, we performed transwell assays to detect the function of TRAF2 in promoting metastasis and explored the correlations between TRAF2, NF-κB, and interleukin-8 (IL-8) in vitro. In addition, we examined the correlation between TRAF2 and tumor microenvironment by immunohistochemistry staining. RESULTS: In our study, we found that TRAF2 expression was markedly increased in gastric cancer tissues. High intratumoral TRAF2 staining, which was associated with tumor invasion and metastasis, was also an independent poor prognosticator for gastric cancer patients. In vitro studies revealed that TRAF2 enhanced NF-κB activation and subsequent IL-8 expression in gastric cancer cells. Inhibition of NF-κB or IL-8 signaling attenuated TRAF2-induced migration and invasion abilities. High TRAF2 expression was confirmed to be associated with both high intratumoral and serum levels of IL-8. In addition, TRAF2 expression was positively correlated with neutrophil and macrophage infiltration as well as microvessels formation in gastric cancer samples. CONCLUSIONS: These results suggest that TRAF2 functions as an important modulator in tumor metastasis and tumor microenvironment formation and is a novel independent prognostic factor of gastric cancer.

Bone Marrow Myeloid Cells Regulate Myeloid-Biased Hematopoietic Stem Cells via a Histamine-Dependent Feedback Loop.

Myeloid-biased hematopoietic stem cells (MB-HSCs) play critical roles in recovery from injury, but little is known about how they are regulated within the bone marrow niche. Here we describe an auto-/paracrine physiologic circuit that controls quiescence of MB-HSCs and hematopoietic progenitors marked by histidine decarboxylase (Hdc). Committed Hdc+ myeloid cells lie in close anatomical proximity to MB-HSCs and produce histamine, which activates the H2 receptor on MB-HSCs to promote their quiescence and self-renewal. Depleting histamine-producing cells enforces cell cycle entry, induces loss of serial transplant capacity, and sensitizes animals to chemotherapeutic injury. Increasing demand for myeloid cells via lipopolysaccharide (LPS) treatment specifically recruits MB-HSCs and progenitors into the cell cycle; cycling MB-HSCs fail to revert into quiescence in the absence of histamine feedback, leading to their depletion, while an H2 agonist protects MB-HSCs from depletion after sepsis. Thus, histamine couples lineage-specific physiological demands to intrinsically primed MB-HSCs to enforce homeostasis.

[Clinicopathologic characteristics and prognosis analysis of 90 young patients with gastric cancer].

OBJECTIVE: To investigate the features of clinicopathology and prognosis in young gastric cancer patients. METHODS: Clinicopathological data of 90 young gastric cancer patients (≤40 years old) who received radical gastrectomy in the Department of General Surgery of Zhongshan Hospital, Fudan University from January 2013 to December 2014 were retrospectively analyzed. Survival data were obtained by follow-up and the last follow-up time was October 2016. Log-rank test and Cox regression model were used to analyze the risk factors of prognosis and these factors included gender, age, tumor size, degree of differentiation, histological type, Lauren pattern, T stage, N stage, vessel carcinoma embolus, clinical symptom, anemic condition, CA19-9 level, et al. RESULTS: The median age of 90 patients was 35 years old, of whom, 20(22.2%) patients were ≤30 years old and 70(77.8%) patients were between 31 and 40 years old. There were 70(77.8%) female patients, 38(42.2%) patients with anemia, 11(12.8%) patients with elevated CA19-9 level and 9(10.0%) patients with family history of gastrointestinal tumors. The mean time of all the patients from presence of symptom to consultation was 8.2 months. Postoperative pathology revealed 65(72.2%) patients with poorly differentiated adenocarcinoma, 6(6.7%) patients with mucinous adenocarcinoma, 9(10%) patients with signet-ring cell carcinoma, and 10(11.1%) patients with papillary-canalicular adencarcinoma. Sixty-nine (76.7%) patients were diagnosed as advanced gastric cancer and 67(74.4%) patients were involved with lymphatic metastasis when they visited our hospital. Univariate analysis showed that gender (P=0.021), tumor size (P=0.001), depth of tumor infiltration (P=0.016), lymphatic metastasis (P=0.000), vessel carcinoma embolus (P=0.001), elevated CA19-9 level (P=0.001), and anemia (0.024) were statistically related with postoperative survival. Multivariate analysis showed that lymphatic metastasis was an independent risk factor of the poor prognosis of young patients (HR:2.774, 95%CI:1.435 to 5.364, P=0.002). CONCLUSIONS: The majority of young gastric cancer cases are female with poorly differentiated adenocarcinoma. Most patients are diagnosed as advanced gastric cancer with lymphatic metastasis when they visit hospital at the first time. The lymphatic metastasis is an independent risk factor of prognosis in young gastric cancer patients.