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Aims The strategy of blood pressure intervention in the elderly hypertensive patients (STEP) trial reported the cardiovascular benefit of intensive systolic blood pressure (SBP) control in patients with hypertension. The association between intensive SBP lowering and the risk of new-onset diabetes is unclear. This study aimed to evaluate the effect of intensive SBP lowering on the incidence of new-onset diabetes. Methods and results Participants in STEP who had baseline fasting serum glucose (FSG) concentrations Conclusion Intensive SBP lowering is not associated with an altered risk of new-onset diabetes or impaired fasting glucose in hypertensive patients. Registration STEP ClinicalTrials.gov, number: NCT03015311.

This study is to investigate the hemorrhagic cystitis (HC) after allogeneic hematopoietic stem cell transplantation (allo-HSCT) without in vitro T-cell depletion. Patients receiving allo-HSCT in 2019 were enrolled. The occurrence and clinical characteristics of HC after HLA-identical HSCT and haploidentical HSCT were retrospectively analyzed. BK, JC, cytomegalovirus, and other viruses were monitored when HC occurred. Conventional HC treatment was performed. Additionally, 5 cases of severe refractory HC were treated with adipose-derived mesenchymal stem cell (ADSC) besides conventional HC treatment. Totally, 54 patients with allo-HSCT were enrolled, including 12 cases with HLA-identical HSCT and 42 cases with haploidentical HSCT. Among them, 17 developed late-onset HC (LOHC). There was no early-onset HC. The median onset time was 33.5 (9-189) days, with a median duration of 19 (5-143) days. There were 8 cases of grade III HC and 2 cases of grade IV HC. The cumulative incidence of LOHC in 54 patients was 29.6%, and the cumulative incidence of LOHC in 42 patients with haploidentical HSCT was 40.5%. The 1-year expected progression-free survival (PFS) of 26 patients without HC was 86.6%, and the 1-year expected PFS of 16 HC patients was 74.5%. However, there was no statistically significant difference (P = .326). The urine BK virus of 14 patients was positive, with the lowest of 1.98 × 105 copies/mL, and the highest of 8.96 × 105 copies/mL. For the 5 patients with severe refractory HC, the lowest infusion dose of ADSC was 0.9 × 106/kg and the highest was 1.4 × 106/kg. All 5 patients were cured. The incidence of LOHC is higher after haploidentical HSCT. LOHC is positively correlated with urine BK virus. LOHC has no obvious effect on the overall PFS of patients. ADSC infusion has a good therapeutic effect on severe and prolonged LOHC.

To determine whether intensive systolic blood pressure (SBP) lowering can benefit hypertensive patients with diabetes.We performed a pooled analysis of individual patient data from two randomized trials to compare intensive and standard SBP targets in hypertensive patients with diabetes (STEP diabetes subgroup and ACCORD-BP standard glycaemic group, n = 1627 and n = 2362, respectively). We defined a modified primary outcome as a composite of stroke, major coronary artery disease (myocardial infarction and unstable angina), heart failure, and cardiovascular death. The secondary outcomes were individual components of the primary outcome and death from any cause. A Cox proportional hazards regression model was used in the main analysis. We conducted one-stage mixed-effect models and two-stage analyses as sensitivity and supplementary analyses to verify the robustness of the findings.A total of 3989 patients were randomized to undergo intensive (n = 1984) or standard SBP treatment (n = 2005). After a median follow-up of 3.83 years, the primary outcome occurred in 193/1984 patients in the intensive group and in 247/2005 patients in the standard group (hazard ratio [HR] 0.77, 95% confidence interval [CI] 0.64-0.93). The incidence rates for secondary outcomes were lower in the intensive group than in the standard group, but were not significantly different, except for stroke (intensive vs. standard: 32/1984 vs. 58/2005; HR 0.56, 95% CI 0.36-0.86). These results remained consistent in the additional sensitivity and supplementary analyses.An intensive SBP-lowering target of 110 to130 mmHg reduces the cardiovascular outcomes compared with a standard SBP-lowering target of 130 to150 mmHg. The findings of this study support the favourable effects of intensive SBP lowering in hypertensive patients with diabetes.

Introduction This study is to investigate the effect of late-onset hemorrhagic cystitis (LOHC) on progression-free survival (PFS) of patients after haploidentical peripheral blood hematopoietic stem cell transplantation (haplo-PBSCT). Methods This retrospective study enrolled 74 patients with hematological malignancies treated with a myeloablative conditioning regimen and haplo-PBSCT. The effect of LOHC on PFS was studied in terms of HC occurrence, grade, disease type, duration, onset time, gender, and age. Results There were 28 patients with LOHC, and no case was with early-onset HC. The cumulative incidence of LOHC was 37.8% (95% CI: 26.9–48.7%). The 2-year expected PFS of 74 patients and 34 AML patients was not significantly different between LOHC patients and patients without HC (P > 0.05). Among 27 ALL patients, the 2-year expected PFS of LOHC patients was 75%, significantly higher than patients without HC (54.2%) (P < 0.05). The 2-year expected PFSs of patients with mild LOHC and severe LOHC were 69.8 and 77.8%, respectively (P > 0.05). Similarly, the onset time, duration, age, and gender of LOHC patients did not show significant effects on PFS (P > 0.05). Conclusions After haplo-PBSCT, LOHC has a significant effect on the PFS of ALL patients. The HC grade, duration, onset time, gender, and age have no significant effect on PFS.

Recent works have extensively probed contextual relevance to enhance the scene understanding. However, most approaches tend to model the relationships between local regions due to the limitation of the convolution kernel, while rarely exploring long-range dependencies. In this paper, we come up with the Dual Context Aggregation Module (DCM) to effectively capture such important information. DCM splits into two attention modules to obtain dense contextual information via modeling relations between positions and channels. The spatial attention module generates huge attention maps by constructing pairwise relationships between positions in the same row or column. The channel attention module applies the Weight Calibrate Block to generate weights for all the channels to effectively get the correlation between different channels. We adopt an element addition to integrate the feature maps of the two modules. Moreover, we design a two-step decoder module to improve the feature representation. On the basis of these developments, we construct the Dual Context aggregation Network (DCNet). Extensive evaluation experiments on the benchmarks prove that our model leads to robust feature representation. Our method demonstrates competitive performance compared to state-of-the-art models, achieving the MIoU scores of 81.9% on Cityscapes and 45.54% on ADE20K.

Image caption is a high-level task in the area of image understanding, in which most of the models adopt a convolutional neural network (CNN) to extract image features assigning a recurrent neural network (RNN) to generate sentences. Researchers tend to design complex networks with deeper layers to improve the performance of feature extraction in recent years. Increasing the size of the network could obtain features of high quality, but it is not an efficient way in terms of computational cost. A large number of parameters brought by CNN makes the research difficult to apply in human daily life. In order to reduce the information loss of the convolutional process with less cost, we propose a lightweight convolutional neural network, named as Bifurcate-CNN (B-CNN). Furthermore, recent works are devoted to generating captions in English, in this paper, we develop an image caption model that generates descriptions in Chinese. Compared with Inception-v3, the depth of our model is shallower with fewer parameters, and the computational cost is lower. Evaluated on the AI CHALLENGER dataset, we prove that our model can enhance the performance, improving BLEU-4 from 46.1 to 49.9 and CIDEr from 142.5 to 156.6 respectively.

MicroRNAs have emerged as key regulators in vascular diseases and are involved in the formation of atherosclerotic lesions. However, the atherosclerotic-specific MicroRNAs and their functional roles in atherosclerosis are unclear. Here, we report that miR-378c protects against atherosclerosis by directly targeting Sterile Alpha Motif Domain Containing 1 (Samd1), a predicted transcriptional repressor. miR-378c was strikingly reduced in atherosclerotic plaques and blood of acute coronary syndrome (ACS) patients relative to healthy controls. Suppression of miR-378c promoted vascular smooth muscle cells (VSMCs) phenotypic transition during atherosclerosis. We also reported for the first time that Samd1 prolonged immobilization of LDL on the VSMCs, thus facilitated LDL oxidation and subsequently foam cell formation. Further, we found that Samd1 contains predicted DNA binding domain and directly binds to DNA regions as a transcriptional repressor. Together, we uncovered a novel mechanism whereby miR-378c-Samd1 circuit participates in two key elements of atherosclerosis, VSMCs phenotypic transition and LDL oxidation. Our results provided a better understanding of atherosclerosis pathophysiology and potential therapeutic management by targeting miR-378c-Samd1 circuit.

Background: The STEP (Strategy of Blood Pressure Intervention in the Elderly Hypertensive Patients) trial reported the cardiovascular benefit of intensive blood pressure (BP) control. The objective of this analysis was to evaluate the effect of intensive BP lowering on the new-onset diabetes incidence. Methods: The patients of STEP who had a baseline fasting serum glucose (FSG) Results: Over a median follow-up of 3.42 years, 273 (9.6%) in the intensive group and 262 (9.5%) in the standard group developed new-onset diabetes (adjusted HR 1.03; 95% CI 0.87-1.22) . The adjusted hazard ratio for the secondary outcome was 1.05 (95% CI 0.92-1.19) . The mean of the highest FSG was 5.82 mmol/l for intensive group and 5.84 mmol/l for standard group. The sensitivity analyses showed no significant difference with respect to the effect of the treatment arms. Conclusions: Intensive BP lowering (target, 110 to Disclosure R. Yang: None. J. Cai: None.

Root and tuber crops are of great importance. They not only contribute to feeding the population but also provide raw material for medicine and small-scale industries. The yield of the root and tuber crops is subject to the development of stem/root tubers, which involves the initiation, expansion, and maturation of storage organs. The formation of the storage organ is a highly intricate process, regulated by multiple phytohormones. Gibberellins (GAs) and abscisic acid (ABA), as antagonists, are essential regulators during stem/root tuber development. This review summarizes the current knowledge of the roles of GA and ABA during stem/root tuber development in various tuber crops.

Hydrostatic pressure, stretch, and shear are major biomechanical forces of vessels and play critical roles in genesis and development of hypertension. Our previous work demonstrated that high hydrostatic pressure (HHP) promoted vascular smooth muscle cells (VSMCs) two novel subsets: inflammatory and endothelial function inhibitory VSMCs and then exacerbated VSMC dysfunction. However, the underlying mechanism remains unknown. Here, we first identified that aortic GPX4 (a core regulator of ferroptosis) significantly downregulated association with VSMC novel phenotype elevation in SHR rats and hypertension patients. In primary VSMCs, HHP (200 mmHg) increased iron accumulation, ROS production, and lipid peroxidation compared with normal pressure (100 mmHg). Consistently, the ferroptosis-related gene (COX-2, TFRC, ACSL4, and NOX-1) expression was also upregulated. The ferroptosis inhibitor ferrostatin-1 (Fer-1) administration blocked HHP-induced VSMC inflammatory (CXCL2 expression) and endothelial function inhibitory (AKR1C2 expression) phenotyping switch association with elevation in the GPX4 expression, reduction in the reactive oxygen species (ROS), and lipid peroxidation production. In contrast, the ferroptosis inducer RLS3 increased HHP-induced CXCL2 and AKR1C2 expressions. These data indicate HHP-triggering ferroptosis contributes to VSMC inflammatory and endothelial function inhibitory phenotyping switch. In mechanism, HHP reduced the VSMC GSH content and cystathionine gamma-lyase (CSE)/hydrogen sulfide (H2S)—an essential system for GSH generation. Supplementation of the H2S donor-NaHS increased the VSMC GSH level, alleviated iron deposit, ROS and lipid peroxidation production. NaHS administration rescues both HHP- and RLS3-induced ferroptosis. Collectively, HHP downregulated VSMC CSE/H2S triggering GSH level reduction, resulting in ferroptosis, which contributed to the genesis of VSMC inflammation and endothelial function inhibitory phenotypes.

Esophageal squamous cell carcinoma (ESCC) is a malignant tumor developing from the esophageal squamous epithelium, and is the most common histological subtype of esophageal cancer (EC). EC ranks 10th in morbidity and sixth in mortality worldwide. The morbidity and mortality rates in China are both higher than the world average. Current treatments of ESCC are surgical treatment, radiotherapy, and chemotherapy. Neoadjuvant chemoradiotherapy plus surgical resection is recommended for advanced patients. However, it does not work in the significant promotion of overall survival (OS) after such therapy. Research on targeted therapy in ESCC mainly focus on EGFR and PD-1, but neither of the targeted drugs can significantly improve the 3-year and 5-year survival rates of disease. Phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway is an important survival pathway in tumor cells, associated with its aggressive growth and malignant progression. Specifically, proliferation, apoptosis, autophagy, and so on. Related genetic alterations of this pathway have been investigated in ESCC, such as PI3K, AKT and mTOR-rpS6K. Therefore, the PI3K/AKT/mTOR pathway seems to have the capability to serve as research hotspot in the future. Currently, various inhibitors are being tested in cells, animals, and clinical trials, which targeting at different parts of this pathway. In this work, we reviewed the research progress on the PI3K/AKT/mTOR pathway how to influence biological behaviors in ESCC, and discussed the interaction between signals downstream of this pathway, especially eukaryotic translation initiation factors (eIFs) and the development and progression of ESCC, to provide reference for the identification of new therapeutic targets in ESCC.

Carp edema virus (CEV) is the pathogen of carp edema virus disease (CEVD), an emerging infectious disease with high morbidity and mortality worldwide. In the winter of 2016, a disease outbreak occurred in a koi pond in Chengdu, located in the southwest of China. The water temperature at that time was 11–13 °C. The clinical signs of the diseased koi were lethargy, unresponsiveness, enophthalmos, swollen gills, and hemorrhagic skin. Histopathological changes were observed in moribund fish, such as significant cell hyperplasia in the gill lamellae, and swelling and vacuolar degeneration in epithelial cells of the renal tubules and hepatocytes. Electron microscopy of renal tissues showed virions of a pox-like virus (200–235 nm diameter). The presence of specific 528 bp and 478 bp fragments was detected by nested PCR. An experimental infection demonstrated cumulative mortality of 15% (3/20) at a water temperature of 13 ± 2 °C. Furthermore, sequence analysis of the partial 4a genes showed that the CEV isolate (MG189372) in this study had 100% homology with a UK strain (KX254027). The evidence showed that the pathogen involved in this outbreak was CEV. To the best of our knowledge, this is the first report of carp disease caused by CEV at low temperature in China, demonstrating that CEV disease should be monitored in the cold season and at low temperatures. The findings are of profound significance to reducing the risk of CEVD outbreaks in carp aquaculture.

The airway epithelium (AE) is the main protective barrier between the host and external environmental factors causing asthma. Allergens or pathogens induce AE dysfunction, including epithelial permeability alteration, trans‑epithelial electrical resistance (TEER) reduction, upregulation of inflammatory mediators and downregulation of junctional complex molecules. Orosomucoid‑like protein isoform 3 (ORMDL3), a gene closely associated with childhood onset asthma, is involved in airway inflammation and remodeling. It was hypothesized that ORMDL3 plays an important role in regulating AE barrier function. In vivo [chronic asthma induced by ovalbumin‑respiratory syncytial virus (OVA‑RSV)] in mice) and in vitro (human bronchial epithelial cells and 16HBE cells) models were used to assess ORMDL3's role in AE function regulation, evaluating paracellular permeability, TEER and the expression levels of junctional complex molecules. The effects of ORMDL3 on the extracellular signal‑regulated protein kinase (ERK) pathway were determined. In mice with OVA‑RSV induced chronic asthma, ORMDL3 and sphingosine kinase 1 (SPHK1) were upregulated whereas the junction related proteins Claudin‑18 and E‑cadherin were downregulated. Overexpression of ORMDL3 resulted in decreased TEER, downregulation of junctional complex molecules and induced epithelial permeability. In contrast, ORMDL3 inhibition showed the opposite effects. In 16HBE cells, ORMDL3 overexpression induced SPHK1 distribution and activity, while SPHK1 inhibition resulted in increased TEER upon administration of an ORMDL3 agonist or ORMDL3 overexpression. In addition, ERK activation occurred downstream of SPHK1 activation in 16HBE cells. High levels of ORMDL3 result in damaged AE barrier function by inducing the SPHK1/ERK pathway.

Introduction Severe hemorrhagic cystitis (HC) is still a common complication after allogeneic hematopoietic stem cell transplantation, which affects the quality of life of patients, and may even cause kidney failure. This study reports the clinical effect of adjuvant treatment of adipose-derived mesenchymal stem cells (ADSCs) on severe refractory HC after of reduced intensity conditioning haplotype high-dose peripheral blood hematopoietic stem cell transplantation (RIC-PBSCT) in one case. Patient concerns A 53-year-old female patient with acute myeloid leukemia (FLT3-ITD) at high risk received RIC-PBSCT. The patient was relieved with complete donor chimerism of 99.01%, and normal hemogram. However, the patient developed frequent urination, urgency, and dysuria with gross hematuria with blood clots and difficult urinating, especially at night and early in the morning. There were obvious hyperemia and bleeding points in the mucosa of the posterior wall of the bladder. Diagnosis The patient was diagnosed as delayed HC of degree IV. Interventions and outcomes The patient was treated with antiviral drugs, urine alkalization, and diuretic drugs for more than 1 month, but no significant effect was obtained. Thus, the patient was then given ADSCs (1 × 106 kg per kg of body weight, infused once a week for a total of 3 infusions). Symptoms of frequent urination, urgency, and dysuria that happened during the first infusion were improved, and blood clots in the urine were also reduced. After the third infusion, HC symptoms disappeared, the red blood cells were normal, and there was no fever, chills, low infusion blood pressure, or rash. The patient's HC was cured. During follow-up, HC recurrence was not observed. Conclusion ADSCs adjuvant treatment of relapsed and refractory severe HC is safe and reliable with good clinical efficacy. It shows certain clinical application value, which however requires more clinical cases to further verify this.

Background: Paired related homeobox 1 (PRRX1) and zinc finger E-box binding homeobox 1 (ZEB1) have been observed to play a vital role in the epithelial-mesenchymal transition (EMT) process in different types of cancer. The microvessel density (MVD) is the most common indicator used to quantify angiogenesis. This study aimed to investigate expression of PRRX1 and ZEB1 in non-small cell lung cancer (NSCLC) and to explore associations between these factors and tumor prognosis, EMT markers and angiogenesis. Methods: Data for a total of 111 surgically resected NSCLC cases from January 2013 to December 2014 were collected. We used an immunohistochemical method to detect expression levels of PRRX1, ZEB1, and E-cadherin, and to assess MVD (marked by CD34 staining). SPSS 26.0 was employed to evaluate the connection between these factors and clinical and histopathological features, overall survival (OS) and tumor angiogenesis. Results: PRRX1 expression was obviously lower in tumor samples than in control samples. Low expression of PRRX1, which was more common in the high-MVD group than in the low-MVD group (P = .009), correlated positively with E-cadherin expression (P

An outbreak of a carp disease occurred in a koi pond in early October 2016, Chengdu, southwest of China. Characteristic signs of infected fish include erratic swimming of moribund fish at the water surface, respiratory distress, presence of thick and foggy mucus covering the body and gills. Skin ulcers were also noticed in a few cases. Microbiological, parasitological and virological investigations were carried out with fish samples collected from various localities. Histologically, the gills, kidney and liver showed discernible changes. By analyzing gill tissues in six samples by PCR and nested-PCR for detection of cyprinid herpesvirus 3 (CyHV-3) and carp edema virus (CEV) respectively, PCR products of 292 bp and 478 bp (by using nested primers) could be amplified. The outbreak of carp disease caused by CEV and CyHV-3 mixed infection was confirmed by sequence analysis of the PCR products. The viral load in the gills and kidney were quantified by real-time TaqMan PCR, which in turn would aid the evaluation of the significance of the virus to the etiology of the disease. The result demonstrated that CEV plays the major role to the death of fish. Phylogenetic analyses revealed that the CEV isolate (GenBank accession no. MG189371) showed closest identity to the CEV isolated from UK (KX254027) with 99% homology. To our knowledge, this is the first report a carp disease caused by CEV and CyHV-3 mixed infection in China.

Background: The tumor with perivascular epithelioid cells (PEComa) is a rare mesenchymal tumor originating from a perivascular epithelioid cell line. The uterus is the most common location of PEComa, but multifocal lesions are rare. This study aimed to analyze the clinicopathologic and histochemical characteristics of uterine PEComa. Methods: 1 case of uterine PEComa was detected by H&E staining and immunohistochemical SP method. Results: The 41-year-old female patient was admitted to the hospital due to gynecologic ultrasonography which showed a substantial heterogeneous mass in the pelvic cavity. According to the microscopic features and immunohistochemical markers, the tumor was diagnosed as multifocal tumors with perivascular epithelioid cells, specifically located on the serous surface of the uterus and below the right appendix. The immunophenotype of the patient was positive for Vimentin, HMB45, TFE-3 and WT-1, but negative for SMA, S-100, CD10, CK, EMA, CD117, CD31 and Melan-A. Conclusion: PEComa is a rare mesenchymal tumor with benign manifestations. Pathological diagnosis should be combined with morphology and immunophenotype. The characteristic immunomarkers are HMB45, Melan-A and SMA. The understanding of clinical manifestations and pathologic features can improve the diagnosis and prevention of this type of tumor in female patients.

Background: Metastasis-associated in colon cancer 1 (MACC1), a candidate oncogene, promotes tumor cell invasion and metastasis in various cancers. Twist1, a key transcriptional gene of the epithelial-mesenchymal transition (EMT), is involved in EMT and metastasis in many cancers. KAI1, also known as CD82, was originally considered as a suppressor gene of tumor metastasis. In this study, we investigated the expressions and significance of MACC1, Twist1, and KAI1 in infiltrating urothelial carcinoma of bladder (IUCB). Methods: The expressions of MACC1, Twist1, and KAI1 in 195 IUCB specimens and their corresponding control specimens were investigated by immunohistochemistry. The patients’ clinical, demographic, and follow-up data were collected. Results: The rates of the positive expressions of MACC1 and Twist1 were significantly higher in IUCB tissues than in normal bladder mucosa tissues, and their expressions were positively correlated with tumor stages, grades of differentiation, lymph node metastasis (LNM), and tumor-node-metastasis (TNM) stages. The rate of positive expression of KAI1 was significantly lower in IUCB than in the control tissues, and its expression was inversely associated with tumor stages, grades of differentiation, LNM, and TNM stages. Patients who expressed MACC1 or Twist1 had an unfavorable overall survival (OS) time when compared with patients who did not express these proteins. However, patients who expressed KAI1 had a favorable OS when compared with patients who did not express this protein. A multivariate analysis demonstrated that the expressions of MACC1, Twist1, and KAI1, tumor stages, grades of differentiation, LNM, as well as TNM stages were independent prognostic indicators for IUCB patients. Conclusion: Therefore, MACC1, Twist1, and KAI1 should be considered potentially promising biomarkers of IUCB prognosis.

Dongzheng Li,1 Ruixue Yang,2 Liu Yang,1 Dongfeng Wang,1 Xin Zhou,1 Yan Sun11Department of General Surgery, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital, Nanjing, Jiangsu 210009, People’s Republic of China; 2Department of Paediatrics, Taikang Xianlin Drum Tower Hospital, Nanjing, Jiangsu 210046, People’s Republic of ChinaBackground: Circular RNAs (circRNAs) and microRNAs (miRNAs) play key roles in the development of human cancers. CircANKS1B has been reported to be increased in breast cancer.Methods: Real-time polymerase chain reaction (real-time PCR) assay was used to measure expressions of circANKS1B, ANKS1B, and FOXM1. Western blot assay was employed to examine the protein level of FOXM1 and Slug. The abilities of cell migration and invasion were measured by wound-healing and transwell assays. The interaction between circANKS1B and miR-149 was confirmed by site-directed mutagenesis and luciferase assays.Results: The expression of circANKS1B was up-regulated in colorectal cancer tissues and cells. Additionally, circANKS1B increased the expression of FOXM1. Furthermore, the enhancement of CRC cell migration and invasion by circANKS1B was dependent on FOXM1. However, previous studies have shown that miR-149 can directly target FOXM1 and act as tumor suppressor in CRC. Consequently, our results showed that miR-149 could directly bind to circANKS1B and FOXM1. The inhibition of circANKS1B could reduce FOXM1 and Slug protein levels, thus suppressing CRC cell migration and invasion.Conclusion: Taken together, circANKS1B promotes colorectal cancer cell migration and invasion by acting as a molecular sponge of miR-149 to modulate FOXM1 and Slug protein levels.Keywords: circANKS1B, cell invasion, miR-149, FOXM1, colorectal cancer

Angiogenic factor with G-patch and FHA domain 1 (AGGF1) is a newly initiator of angiogenesis. Forkhead box C2 (FOXC2) that is a member of the winged spiral transcription factor family plays an important role in epithelial-mesenchymal transition (EMT). Epithelial-cadherin (E-cad) that is an adhesion molecule is also involved in EMT. The purpose of this study is to investigate the expression of AGGF1, FOXC2, and E-cad in esophageal squamous cell carcinoma (ESCC) and their clinical significance. Immunohistochemistry was performed to investigate the expression of AGGF1, FOXC2, and E-cad in 170 ESCC specimens and corresponding normal esophageal mucosa tissues. Follow-up data was also collected. The positive rates of AGGF1 and FOXC2 expression were significantly higher in ESCC group when compared with the control group; the positive rate of E-cad expression was significantly lower in ESCC group when compared with the control group. Positive rates of AGGF1, FOXC2, and E-cad expression were significantly associated with grades of differentiation, tumor grades, lymph node metastasis stages, as well as tumor-node-metastasis stages. Kaplan–Meier analysis demonstrated that positive expression of AGGF1 or FOXC2 for ESCC patients had significantly unfavorably overall survival time when compared with patients with negative expression of AGGF1 or FOXC2; and positive expression of E-cad for ESCC patients had significantly longer overall survival time when compared with patients with negative expression of E-cad. Multivariate analysis indicated that AGGF1, FOXC2, and E-cad expression and tumor-node-metastasis stages were postoperative independent prognostic factors for ESCC patients. AGGF1, FOXC2, and E-cad may be considered promising biomarkers of ESCC patients’ prognosis.