Objective:To investigate the mechanism of ursolic acid (UA) in inhibiting the growth and metastasis of breast cancer MDA-MB-231 (“231”) cells by downregulating ANXA6.Methods:This study conducted relevant in vitro cytology and molecular biology experiments in the Department of Clinical Laboratory and Central Laboratory of Putuo Hospital, Shanghai University of Traditional Chinese Medicine from February 2023 to August 2024. Human breast cancer 231 cells were cultured in vitro, and the effects of different concentrations of UA on the proliferation and invasion and metastasis of 231 cells were detected by CCK-8 and Transwell assays. Western Blot was used to detect the effect of UA on the expression of ANXA6 and invasion and metastasis-related proteins MMP9, β-catenin and N-cadherin in 231 cells. The 231 cells that interfered with and overexpressed ANXA6 were constructed by lentivirus transfection to generate stable ANXA6 interfering and overexpressing 231 cells, which were divided into 231/KD-ANXA6 group, 231/KD-NC group, 231/OE-ANXA6 group, and 231/OE-NC group. CCK-8 assay and Transwell assay were used to detect the proliferation activity, invasion and metastasis ability of 231 cells after interference and overexpression of ANXA6 and the effect of UA on the proliferation ability of 231 cells after interference and overexpression of ANXA6. Western Blot and RT-PCR assays were used to detect the expression of invasion and migration biomarkers such as MMP9, β-catenin, and N-cadherin in 231 cells after interference and overexpression of ANXA6. Immunohistochemistry was used to detect the expression level of ANXA6 in breast cancer tissues, and the relationship between ANXA6 expression and clinicopathological features and prognosis of breast cancer was analyzed.Results:The CCK-8 assay results showed that compared with the control group (0 μmol/L UA, 100.00%±7.37%), the proliferative activity of 231 cells at UA concentrations of 2.5, 5, 10, 20 and 40 μmol/L (90.23%±1.76%, t=2.24, P<0.05; 85.19%±4.23%, t=3.02, P<0.05; 65.45%±0.35%, t=8.11, P<0.01; 37.79%±0.98%, t=14.50, P<0.001; 18.18%±0.15%, t=19.23, P<0.001) were significantly decreased. Furthermore, UA (10, 15, 20 μmol/L) inhibited the invasion and metastasis ability of 231 cells; Western Blot assay showed that compared with the control group (0 μmol/L UA), the protein expressions of MMP9 (1.07±0.03 vs 0.99±0.11, t=1.27, P>0.05), β-catenin (1.21±0.01 vs 0.99±0.07, t=5.47, P<0.05), N-cadherin (1.05±0.09 vs 0.90±0.03, t=2.65, P>0.05) at UA of 10 μmol/L; MMP9 (1.07±0.03 vs 0.79±0.09, t=5.26, P<0.001), β-catenin (1.21±0.01 vs 0.89±0.05, t=10.55, P<0.001), and N-cadherin (1.04±0.09 vs 0.68±0.10, t=4.59, P<0.05) at UA of 15 μmol/L; MMP9 (1.07±0.03 vs 0.52±0.07, t=12.50, P<0.001), β-catenin (1.21±0.01 vs 0.83±0.02, t=24.01, P<0.000 1) and N-cadherin (1.04±0.09 vs 0.49±0.11, t=6.70, P<0.01) at UA of 20 μmol/L. Interfering with ANXA6 inhibits the proliferation, invasion and migration of 231 cells, and overexpression of ANXA6 promotes the proliferation, invasion and migration of 231 cells. Western Blot assay showed that compared with the control group (KD-NC group), the protein expressions of MMP9 (1.07±0.01 vs 0.62±0.16, t=4.86, P<0.01), β-catenin (1.02±0.14 vs 0.64±0.15, t=3.20, P<0.05), N-cadherin (0.98±0.14 vs 0.67±0.12, t=2.85, P<0.05) were decreased expression; Compared with the control group (OE-NC group), the protein expressions of MMP9 (0.54±0.22 vs 1.06±0.08, t=3.90, P<0.05), β-catenin (0.92±0.07 vs 1.06±0.04, t=3.06, P<0.05) and N-cadherin (0.90±0.07 vs 1.06±0.01, t=3.75, P<0.05) were significantly increased. Interference with ANXA6 promoted the inhibitory effect of UA on the proliferation ability of 231 cells ( P<0.05). Overexpression of ANXA6 weakened the inhibitory effect of UA on the proliferation of 231 cells ( P<0.05).The results of immunohistochemistry assay showed that the expression level of ANXA6 in breast cancer tissue was significantly increased, and the expression of ANXA6 was related to tumor size ( P<0.05), but not to age, T stage, N stage, pathological grade, AJCC stage, ER, PR and E-cad. Conclusion:The expression level of ANXA6 in breast cancer tissues is increased, and UA can inhibit the growth, invasion and metastasis of 231 cells by down-regulating the expression of ANXA6.

Objective To investigate the effect of long non-coding RNA small nucleolar RNA host gene 14(LncRNA SNHG14)on high glucose-induced podocyte injury by targeting microRNA-30a-5p(miR-30a-5p).Methods Podocytes were cultured in vitro and were divided into the following groups:the standard glucose(NG)group,the high glucose(HG)group,the si-NC+HG group,the si-SNHG14+HG group,the miR-NC+HG group,the miR-30a-5p mimics+HG group,the si-SNHG14+inhibitor NC+HG group and the si-SNHG14+miR-30a-5p inhibitor+HG group.Quantitative real-time polymerase chain reaction(RT-qPCR)was performed to detect expression levels of LncRNA SNHG14 and miR-30a-5p.Flow cytometry was used to determine cell apoptosis.Enzyme-linked immunosorbent assay(ELISA)was applied to measure levels of tumor necrosis factor-alpha(TNF-α),interleukin(IL)-6 and IL-1β.Xanthine oxidase method,ammonium molybdate colorimetry and thiobarbituric acid method were respectively used to detect superoxide dismutase(SOD),catalase(CAT)and malondialdehyde(MDA).Dual-luciferase reporter gene was conducted to verify the targeting relationship between LncRNA SNHG14 and miR-30a-5p.Western blot assay was performed to detect expression levels of apoptosis-related proteins.Results Compared with the NG group,the HG group exhibited increased expression levels of LncRNA SNHG14,cell apoptosis rate,as well as levels of TNF-α,IL-6,IL-1β and MDA,whereas the expression level of miR-30a-5p and levels of SOD and CAT were decreased(P＜0.05).Compared with the HG group and the si-NC+HG group,the si-SNHG14+HG group exhibited decreased expression levels of LncRNA SNHG14,apoptosis rate,levels of TNF-α,IL-6,IL-1β and MDA,as well as expression levels of Bax and cleaved caspase-3 proteins,while the expression level of miR-30a-5p,levels of SOD and CAT and the expression level of Bcl-2 protein were increased(P＜0.05).Compared with the HG group and the miR-NC+HG group,the miR-30a-5p mimics+HG group showed no significant difference in the expression level of LncRNA SNHG14(P＞0.05).Meanwhile,the expression level of miR-30a-5p,levels of SOD and CAT,and expression level of Bcl-2 protein were increased,whereas the cell apoptosis rate,levels of TNF-α,IL-6,IL-1β and MDA,as well as expression levels of Bax and cleaved caspase-3 proteins were decreased(P＜0.05).Compared with the si-SNHG14+HG group and the si-SNHG14+inhibitor NC+HG group,the si-SNHG14+miR-30a-5p inhibitor+HG group showed no significant difference in the expression level of LncRNA SNHG14(P＞0.05),meanwhile,the expression level of miR-30a-5p,levels of SOD and CAT,and expression level of Bcl-2 protein were reduced,whereas the cell apoptosis rate,levels of TNF-α,IL-6,IL-1β and MDA,as well as expression levels of Bax and cleaved caspase-3 proteins were increased(P＜0.05).The dual-luciferase reporter gene assay confirmed that LncRNA SNHG14 targeted and negatively regulated miR-30a-5p.Conclusion The inhibition of LncRNA SNHG14 can target miR-30a-5p to alleviate high glucose induced podocyte injury.

Objective:To investigate the mechanism of ursolic acid (UA) in inhibiting the growth and metastasis of breast cancer MDA-MB-231 (“231”) cells by downregulating ANXA6.Methods:This study conducted relevant in vitro cytology and molecular biology experiments in the Department of Clinical Laboratory and Central Laboratory of Putuo Hospital, Shanghai University of Traditional Chinese Medicine from February 2023 to August 2024. Human breast cancer 231 cells were cultured in vitro, and the effects of different concentrations of UA on the proliferation and invasion and metastasis of 231 cells were detected by CCK-8 and Transwell assays. Western Blot was used to detect the effect of UA on the expression of ANXA6 and invasion and metastasis-related proteins MMP9, β-catenin and N-cadherin in 231 cells. The 231 cells that interfered with and overexpressed ANXA6 were constructed by lentivirus transfection to generate stable ANXA6 interfering and overexpressing 231 cells, which were divided into 231/KD-ANXA6 group, 231/KD-NC group, 231/OE-ANXA6 group, and 231/OE-NC group. CCK-8 assay and Transwell assay were used to detect the proliferation activity, invasion and metastasis ability of 231 cells after interference and overexpression of ANXA6 and the effect of UA on the proliferation ability of 231 cells after interference and overexpression of ANXA6. Western Blot and RT-PCR assays were used to detect the expression of invasion and migration biomarkers such as MMP9, β-catenin, and N-cadherin in 231 cells after interference and overexpression of ANXA6. Immunohistochemistry was used to detect the expression level of ANXA6 in breast cancer tissues, and the relationship between ANXA6 expression and clinicopathological features and prognosis of breast cancer was analyzed.Results:The CCK-8 assay results showed that compared with the control group (0 μmol/L UA, 100.00%±7.37%), the proliferative activity of 231 cells at UA concentrations of 2.5, 5, 10, 20 and 40 μmol/L (90.23%±1.76%, t=2.24, P<0.05; 85.19%±4.23%, t=3.02, P<0.05; 65.45%±0.35%, t=8.11, P<0.01; 37.79%±0.98%, t=14.50, P<0.001; 18.18%±0.15%, t=19.23, P<0.001) were significantly decreased. Furthermore, UA (10, 15, 20 μmol/L) inhibited the invasion and metastasis ability of 231 cells; Western Blot assay showed that compared with the control group (0 μmol/L UA), the protein expressions of MMP9 (1.07±0.03 vs 0.99±0.11, t=1.27, P>0.05), β-catenin (1.21±0.01 vs 0.99±0.07, t=5.47, P<0.05), N-cadherin (1.05±0.09 vs 0.90±0.03, t=2.65, P>0.05) at UA of 10 μmol/L; MMP9 (1.07±0.03 vs 0.79±0.09, t=5.26, P<0.001), β-catenin (1.21±0.01 vs 0.89±0.05, t=10.55, P<0.001), and N-cadherin (1.04±0.09 vs 0.68±0.10, t=4.59, P<0.05) at UA of 15 μmol/L; MMP9 (1.07±0.03 vs 0.52±0.07, t=12.50, P<0.001), β-catenin (1.21±0.01 vs 0.83±0.02, t=24.01, P<0.000 1) and N-cadherin (1.04±0.09 vs 0.49±0.11, t=6.70, P<0.01) at UA of 20 μmol/L. Interfering with ANXA6 inhibits the proliferation, invasion and migration of 231 cells, and overexpression of ANXA6 promotes the proliferation, invasion and migration of 231 cells. Western Blot assay showed that compared with the control group (KD-NC group), the protein expressions of MMP9 (1.07±0.01 vs 0.62±0.16, t=4.86, P<0.01), β-catenin (1.02±0.14 vs 0.64±0.15, t=3.20, P<0.05), N-cadherin (0.98±0.14 vs 0.67±0.12, t=2.85, P<0.05) were decreased expression; Compared with the control group (OE-NC group), the protein expressions of MMP9 (0.54±0.22 vs 1.06±0.08, t=3.90, P<0.05), β-catenin (0.92±0.07 vs 1.06±0.04, t=3.06, P<0.05) and N-cadherin (0.90±0.07 vs 1.06±0.01, t=3.75, P<0.05) were significantly increased. Interference with ANXA6 promoted the inhibitory effect of UA on the proliferation ability of 231 cells ( P<0.05). Overexpression of ANXA6 weakened the inhibitory effect of UA on the proliferation of 231 cells ( P<0.05).The results of immunohistochemistry assay showed that the expression level of ANXA6 in breast cancer tissue was significantly increased, and the expression of ANXA6 was related to tumor size ( P<0.05), but not to age, T stage, N stage, pathological grade, AJCC stage, ER, PR and E-cad. Conclusion:The expression level of ANXA6 in breast cancer tissues is increased, and UA can inhibit the growth, invasion and metastasis of 231 cells by down-regulating the expression of ANXA6.

Objective To investigate the effect of long non-coding RNA small nucleolar RNA host gene 14(LncRNA SNHG14)on high glucose-induced podocyte injury by targeting microRNA-30a-5p(miR-30a-5p).Methods Podocytes were cultured in vitro and were divided into the following groups:the standard glucose(NG)group,the high glucose(HG)group,the si-NC+HG group,the si-SNHG14+HG group,the miR-NC+HG group,the miR-30a-5p mimics+HG group,the si-SNHG14+inhibitor NC+HG group and the si-SNHG14+miR-30a-5p inhibitor+HG group.Quantitative real-time polymerase chain reaction(RT-qPCR)was performed to detect expression levels of LncRNA SNHG14 and miR-30a-5p.Flow cytometry was used to determine cell apoptosis.Enzyme-linked immunosorbent assay(ELISA)was applied to measure levels of tumor necrosis factor-alpha(TNF-α),interleukin(IL)-6 and IL-1β.Xanthine oxidase method,ammonium molybdate colorimetry and thiobarbituric acid method were respectively used to detect superoxide dismutase(SOD),catalase(CAT)and malondialdehyde(MDA).Dual-luciferase reporter gene was conducted to verify the targeting relationship between LncRNA SNHG14 and miR-30a-5p.Western blot assay was performed to detect expression levels of apoptosis-related proteins.Results Compared with the NG group,the HG group exhibited increased expression levels of LncRNA SNHG14,cell apoptosis rate,as well as levels of TNF-α,IL-6,IL-1β and MDA,whereas the expression level of miR-30a-5p and levels of SOD and CAT were decreased(P＜0.05).Compared with the HG group and the si-NC+HG group,the si-SNHG14+HG group exhibited decreased expression levels of LncRNA SNHG14,apoptosis rate,levels of TNF-α,IL-6,IL-1β and MDA,as well as expression levels of Bax and cleaved caspase-3 proteins,while the expression level of miR-30a-5p,levels of SOD and CAT and the expression level of Bcl-2 protein were increased(P＜0.05).Compared with the HG group and the miR-NC+HG group,the miR-30a-5p mimics+HG group showed no significant difference in the expression level of LncRNA SNHG14(P＞0.05).Meanwhile,the expression level of miR-30a-5p,levels of SOD and CAT,and expression level of Bcl-2 protein were increased,whereas the cell apoptosis rate,levels of TNF-α,IL-6,IL-1β and MDA,as well as expression levels of Bax and cleaved caspase-3 proteins were decreased(P＜0.05).Compared with the si-SNHG14+HG group and the si-SNHG14+inhibitor NC+HG group,the si-SNHG14+miR-30a-5p inhibitor+HG group showed no significant difference in the expression level of LncRNA SNHG14(P＞0.05),meanwhile,the expression level of miR-30a-5p,levels of SOD and CAT,and expression level of Bcl-2 protein were reduced,whereas the cell apoptosis rate,levels of TNF-α,IL-6,IL-1β and MDA,as well as expression levels of Bax and cleaved caspase-3 proteins were increased(P＜0.05).The dual-luciferase reporter gene assay confirmed that LncRNA SNHG14 targeted and negatively regulated miR-30a-5p.Conclusion The inhibition of LncRNA SNHG14 can target miR-30a-5p to alleviate high glucose induced podocyte injury.

As a representative chemotherapeutic drug, docetaxel (DTX) has been used for breast cancer treatment for decades. However, the poor solubility of DTX limits its efficacy, and the DTX based therapy increases the metastasis risk due to the upregulation of C-X-C chemokine receptor type 4 (CXCR4) expression during the treatment. Herein, we conjugated CXCR4 antagonist peptide (CTCE) with DTX (termed CTCE-DTX) as an anti-metastasis agent to treat breast cancer. CTCE-DTX could self-assemble to nanoparticles, targeting CXCR4-upregulated metastatic tumor cells and enhancing the DTX efficacy. Thus, the CTCE-DTX NPs achieved promising efficacy on inhibiting both bone-specific metastasis and lung metastasis of triple-negative breast cancer. Our work provided a rational strategy on designing peptide-drug conjugates with synergistic anti-tumor efficacy.

Objective: To investigate the ameliorative effects of Mushroom on adipose tissue inflammation and glucolipid metabolism in mice fed a high-fat diet, and to provide a theoretical basis for the mechanisms of Mushroom regulating glucolipid metabolism and inflammatory responses. Methods: C57 BL/6 J mice were fed with normal diet(LF) group, high-fat diet(HF)group and high-fat diet + Mushroom(HF+Mushroom) group for 15 weeks.Then, body weight subcutaneous and epididymal white adipose tissue weight were measured. The morphological changes of adipose tissues were compared by HE staining, and the expression of genes related to inflamation, glycolysis and fatty acid oxidation pathways were detected by RT-PCR and Western blot. Results: Compared with the LF group, the HF group had increased body weight, increased subcutaneous and epididymal white fat weight and adipocyte size, and upregulated expression of tumor necrosis factor-α(TNF-α), interleukin-6(IL-6), monocyte chemoattractant protein-1(MCP-1), CD68, inducible nitric oxide synthase(iNOS), pyruvate kinase(PK), phosphofructokinase(PFK), hypoxia inducible factor-1α(HIF-1α) and peroxisome proliferator activated receptor alpha(PPARα) in adipose tissues, while the expression of carnitine palmitoyl transferase-1 A(CPT-1 A), cytochrome P450 4 a10(CYP4 a10) and medium-chain acyl-coenzyme a dehydrogenase(MCAD) were downregulated(P<0.05). Compared with the HF group, Mushroom supplementation reduced body weight, adipose tissue weight and adipocyte size, and downregulated the expression of pro-inflammatory factors and glycolytic pathway-related factors in adipose tissues, while the expression of fatty acid oxidation pathway-related factors were upregulated(P<0.05). Conclusion Mushroom can ameliorate inflammation and disorders of glycolipid metabolism in adipose tissues of obese mice.

BACKGROUND: Research on the relationship between residential altitude and hypertension incidence has been inconclusive. Evidence at low altitudes (i.e., <1,500 m) is scarce, let alone in older adults, a population segment with the highest hypertension prevalence. Thus, the objective of this study is to determine whether hypertension risk may be affected by altitude in older adults living at low altitudes. METHODS: This prospective cohort study collected data from the Chinese Longitudinal Healthy Longevity Survey (CLHLS). We selected 6,548 older adults (≥65 years) without hypertension at baseline (2008) and assessed events by the follow-up surveys done in 2011, 2014, and 2018 waves. The mean altitude of 613 residential units (county or district) in which the participants resided was extracted from the Digital Elevation Model (DEM) of the National Aeronautics and Space Administration (NASA) and was accurate to within 30 m. The Cox regression model with penalized splines examined the linear or nonlinear link between altitude and hypertension. A random-effects Cox regression model was used to explore the linear association between altitude and hypertension. RESULTS: The overall rate of incident hypertension was 8.6 per 100-person years. The median altitude was 130.0 m (interquartile range [IQR] = 315.5 m). We observed that the exposure-response association between altitude and hypertension incidence was not linear. The shape of the exposure-response curve showed that three change points existed. Hypertension risk increased from the lowest to the first change point (247.1 m) and slightly fluctuated until the last change point (633.9 m). The risk decreased above the last change point. According to the categories stratified by the change points, altitude was only significantly associated with hypertension risk (hazard ratio [HR] = 1.003; 95% confidence interval [CI] = 1.002-1.005) under the first change point (247.1 m) after adjusting for related covariates. CONCLUSION Our study found that the association between altitude and hypertension risk might not be linear. We hope the further study can be conducted to confirm the generality of our findings.
Aged ; Altitude ; Humans ; Hypertension/etiology* ; Incidence ; Prevalence ; Prospective Studies

Objective:To investigate the status quo of knowledge, belief and practice level of nurses on venous access device in three Class Ⅲ Grade A hospitals in Shandong Province and to analyze the influencing factors.Methods:Using the convenient sampling method, a total of 396 nurses from three ClassⅢ Grade A hospitals in Shandong Province were selected as the research objects from June to August 2020. The survey was conducted using the general information questionnaire, Nurses' Knowledge, Belief and Practice Scale on Venous Access Device, Nursing Work Environment Scale and Chinese Registered Nurses Ability Evaluation Scale. Univariate and multivariate analysis were used to analyze the influencing factors of knowledge, belief and practice of nurses on venous access devices. In this study, a total of 396 questionnaires were sent out and 385 were effectively received, with a valid recovery rate of 97.2%.Results:The total scores of Nurses' Knowledge, Belief and Practice Scale on Venous Access Device, Nursing Work Environment Scale and Chinese Registered Nurses Ability Evaluation Scale for 385 nurses in three Class Ⅲ Grade A hospitals were respectively (124.37±16.89) , (98.72±11.32) and (132.04±19.84) . The results of hierarchical regression analysis showed that after controlling for general data, the working environment and the core competence of nurses were important factors that affected the knowledge, belief and practice of nurses on venous access devices, which could explain 40.8% of the total variation of nurses' knowledge, belief and practice on venous access devices.Conclusions:In this study, the knowledge, belief and practice level of nurses on venous access devices in three ClassⅢ Grade A hospitals in Shandong Province is at a medium level, which is affected by a variety of factors. Nursing managers should pay attention to the improvement of nurses' core competence and working environment, so as to enhance their knowledge, belief and practice level of venous access devices and reduce the incidence of complications of venous access devices.

Objective The objective of this study was to investigate the expression of P28 and P43 in papillary thyroid carcinoma(PTC)and its relationship with clinicopathological features after TRa1 gene transcription.Methods Real-time fluorescence quantitative PCR(RT-PCR)and gel electrophoresis were used to determine the target fragments and to isolate the bands of different fragments.The optical density of each band was scanned by UV transmittance analyzer to detect 31 cases of PTC tissue and expression levels of P28 and P43 in para-cancerous tissues.Results The average gray value of P28 in thyroid carcinoma group was 0.77±0.34,which was significantly higher than that in para-cancer group(0.31±0.18).The average gray value of P43(0.85+0.21)in thyroid carcinoma group was significantly higher than that in para-cancer group(0.34±0.15)(P<0.05).The expression levels of P28 were not correlated with gender,age,tumor size,lymph node metastasis and clinical pathologic stage(P>0.05),The expression levels of P43 were not correlated with gender,age,tumor size and lymph node metastasis.(P>0.05)but they were related to clinical pathologic stage(P<0.05).There was no correlation between expression levels of P28 and P43(r=0.266,P=0.071).Conclusion The increased expression of P28 and P43 may have a high degree of malignancy and a certain clinical value in predicting the adverse prognosis of PTC.Both factors are helpful for the prevention and treatment of PTC.

Aim TostudytheeffectsofCuO,ZnOand TiO2 nanoparticles on the viability and metastatic po-tential of EC-9706 and EC-109 esophageal squamous carcinomacelllineinvitro.Methods Characteristics of CuO,ZnO and TiO2 nanoparticles were detected u-sing transmission electron microscope (TEM)and dy-namic light scattering (DLS ).EC-9706 and EC-109 cells were treated with different concentrations of CuO, ZnO and TiO2 (5 ~80 mg · L-1 ).The cell prolifera-tion was analyzed by MTT assay.The cell cycle and apoptotic rates were determined by flow cytometry (FCM).The cell invasion was assayed in Transwell chambers.The expression of Bcl-2 and caspase-3 pro-tein in cells was detected by Western blot method.Re-sults CuO,ZnOandTiO2nanoparticleswerespheri-cal with primary particle size 12,20. 6,12 nm.The particles were agglomerated in water and cell culture medium with negative charge.CuO and ZnO nanoparti-cles induced decreases in EC-9706 and EC-109 cell vi-ability dose-dependently.After exposed to increasing concentrations of CuO and ZnO nanoparticles,the cell cycle analysis revealed a decreasing proportion of cells in G2/Mand S phase,and up-regulation of the cells in G0/G1 phase.Apoptotic cells also increased along with decreased cell invasion upon CuO and ZnO treatment. Nanoparticles treatment after 48 h, the activated caspase-3 expression quantity increased significantly and the Bcl-2 expression quantity decreased obviously (P<0. 05 )compared with control group.TiO2 nanop-articles had no obvious effect on the EC-9706 and EC-109 cell proliferation,cell cycle,apoptosis and inva-sion.Conclusion ComparedwithTiO2,CuOand ZnO nanoparticles can inhibit EC-9706 and EC-109 cell viability and metastatic potential,the mechanism of action involves cell cycle arrest in G0/G1 phase and apoptosis.These findings can help the development of nanoparticles as anti-cancer therapeutics for esophageal cancer.