Objective To enhance the gamma spectrometry analysis and detection capabilities of personnel in measuring radionuclides in bio-ash, and ensure the accuracy and precision of gamma spectrometer in our laboratory for the analysis of radionuclides in bio-ash. Methods The laboratory participated in the 2024 national interlaboratory comparison for radionuclide measurement in bio-ash. Radionuclides ²⁴¹Am, ¹³⁷Cs, and ⁴⁰K in four different bio-ash samples were measured. Based on the measurement methods specified in GB/T 16145—2022, sample measurement, result calculation, and uncertainty evaluation were performed using spectrometry analysis software and sourceless efficiency calibration software. The measurement results and performance evaluation of the laboratory in the comparison were analyzed, and factors affecting gamma-spectrometry measurement and result interpretation were discussed. Results The relative deviation (D) of the measurement results for radionuclides ²⁴¹Am and ¹³⁷Cs in the four bio-ash samples ranged from −10.2% to 2.0% and −1.7% to 0.3%, respectively. The P statistic ranged from 7.0% to 12.5% and 5.0% to 10.8%, respectively. These results met the criteria of |D| ≤ 20% (MARB), |D| ≤ 2.58P, and P ≤ 20% (MARB). The ζ-scores for the measurement of ⁴⁰K in the four bio-ash samples ranged from 0.8 to 1.3, satisfying the criterion of |ζ| < 2. All measurement results in this laboratory in the comparison were satisfactory. Conclusion The laboratory uses a high-purity germanium gamma spectrometer to measure radionuclides in bio-ash. The self-absorption correction method, analysis method, and uncertainty evaluation are appropriate, which can ensure the accuracy and precision of the measurement results. The measurement results are accurate and reliable.

ObjectiveTo investigate the effects and potential mechanisms of Babaodan （BBD） against acetaminophen （APAP）-induced acute liver injury （ALI） based on transcriptomics. MethodsA total of 36 male C57BL/6 mice were randomly divided into 6 groups （n=6 per group）： normal group， model group， N-acetylcysteine group （NAC， 120 mg·kg^-1）， and BBD low-， medium-， and high-dose groups （BBD-L， BBD-M， BBD-H groups， 75， 150， 300 mg·kg^-1， respectively）. Except for the normal group， all other groups were subjected to APAP-induced ALI. The serum levels of aspartate aminotransferase （AST）， alanine aminotransferase （ALT）， total cholesterol （TC）， triglyceride （TG）， and low-density lipoprotein cholesterol （LDL-C） were measured in each group. Hepatic levels or activities of malondialdehyde （MDA） and glutathione peroxidase （GSH-Px） were detected using commercial kits. Hematoxylin-eosin （HE） staining was performed to evaluate the degree of liver histopathological damage. Transcriptomic analysis was employed to screen differentially expressed genes （DEGs）， and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis was performed to identify differential pathways involved in BBD intervention against ALI. Real-time quantitative polymerase chain reaction （Real-time PCR） and Western blot were applied to validate the expression of differential genes and related pathway proteins. Additionally， glucose （GLU） consumption， as well as lactate （LD） and adenosine triphosphate （ATP） content were assessed across all mouse groups. ResultsPharmacodynamic evaluation showed that， compared with the normal group， the model group exhibited significantly elevated serum levels of ALT， AST， TC， TG， and LDL-C （P<0.01）， significantly increased MDA level （P<0.01）， and significantly decreased GSH-Px level （P<0.05）. Compared with the model group， BBD intervention at different doses significantly reduced the serum levels of ALT， AST， TC， TG， and LDL-C （P<0.05， P<0.01）， increased GSH-Px level （P<0.05， P<0.01）， significantly decreased MDA level （P<0.01）， and ameliorated hepatic histopathological injury. Liver transcriptomic analysis revealed that， following high-dose BBD intervention， the core genes were mainly enriched in pathways related to inflammatory responses and energy metabolic reprogramming， including the interleukin-17 （IL-17） signaling pathway， the phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway， fructose and mannose metabolism， and glycolysis. Real-time PCR validation demonstrated that， compared with the normal group， the mRNA expression levels of glycolysis-related genes ［hexokinase 1 （HK1）， hexokinase 2 （HK2）， 6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 3 （PFKFB3）， 6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 4 （PFKFB4）， pyruvate kinase M （PKM）， and lactate dehydrogenase A （LDHA）］， as well as inflammatory cytokines ［tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， and interleukin-1β （IL-1β）］ were significantly upregulated in the model group （P<0.05， P<0.01）. Compared with the model group， the BBD-H group showed significantly decreased mRNA expression of HK1， HK2， PFKFB3， PFKFB4， PKM， LDHA， TNF-α， IL-6， and IL-1β （P<0.05， P<0.01）. Western blot results indicated that， compared with the normal group， the model group had significantly increased expression of glycolysis-related proteins ［glucose transporter 1 （GLUT1）， HK1， PFKFB3， and PKM］， inflammatory proteins ［interleukin-18 （IL-18）， TNF-α， and IL-1β］， and phosphorylated （p）-PI3K and p-Akt proteins （P<0.05， P<0.01）. Compared with the model group， the BBD-H group exhibited significantly decreased expression of GLUT1， HK1， PFKFB3， PKM， IL-18， TNF-α， IL-1β， p-PI3K， and p-Akt （P<0.05， P<0.01）. Metabolic indicator measurements showed that， compared with the model group， the BBD-H group showed significantly reduced GLU consumption， LD and ATP content （P<0.05， P<0.01）. ConclusionBBD may alleviate APAP-induced ALI through dual regulation of metabolic reprogramming and inflammatory responses， potentially via inhibition of the PI3K/Akt signaling pathway.

ObjectiveTo investigate the effects and potential mechanisms of Babaodan （BBD） against acetaminophen （APAP）-induced acute liver injury （ALI） based on transcriptomics. MethodsA total of 36 male C57BL/6 mice were randomly divided into 6 groups （n=6 per group）： normal group， model group， N-acetylcysteine group （NAC， 120 mg·kg^-1）， and BBD low-， medium-， and high-dose groups （BBD-L， BBD-M， BBD-H groups， 75， 150， 300 mg·kg^-1， respectively）. Except for the normal group， all other groups were subjected to APAP-induced ALI. The serum levels of aspartate aminotransferase （AST）， alanine aminotransferase （ALT）， total cholesterol （TC）， triglyceride （TG）， and low-density lipoprotein cholesterol （LDL-C） were measured in each group. Hepatic levels or activities of malondialdehyde （MDA） and glutathione peroxidase （GSH-Px） were detected using commercial kits. Hematoxylin-eosin （HE） staining was performed to evaluate the degree of liver histopathological damage. Transcriptomic analysis was employed to screen differentially expressed genes （DEGs）， and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis was performed to identify differential pathways involved in BBD intervention against ALI. Real-time quantitative polymerase chain reaction （Real-time PCR） and Western blot were applied to validate the expression of differential genes and related pathway proteins. Additionally， glucose （GLU） consumption， as well as lactate （LD） and adenosine triphosphate （ATP） content were assessed across all mouse groups. ResultsPharmacodynamic evaluation showed that， compared with the normal group， the model group exhibited significantly elevated serum levels of ALT， AST， TC， TG， and LDL-C （P<0.01）， significantly increased MDA level （P<0.01）， and significantly decreased GSH-Px level （P<0.05）. Compared with the model group， BBD intervention at different doses significantly reduced the serum levels of ALT， AST， TC， TG， and LDL-C （P<0.05， P<0.01）， increased GSH-Px level （P<0.05， P<0.01）， significantly decreased MDA level （P<0.01）， and ameliorated hepatic histopathological injury. Liver transcriptomic analysis revealed that， following high-dose BBD intervention， the core genes were mainly enriched in pathways related to inflammatory responses and energy metabolic reprogramming， including the interleukin-17 （IL-17） signaling pathway， the phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway， fructose and mannose metabolism， and glycolysis. Real-time PCR validation demonstrated that， compared with the normal group， the mRNA expression levels of glycolysis-related genes ［hexokinase 1 （HK1）， hexokinase 2 （HK2）， 6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 3 （PFKFB3）， 6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 4 （PFKFB4）， pyruvate kinase M （PKM）， and lactate dehydrogenase A （LDHA）］， as well as inflammatory cytokines ［tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， and interleukin-1β （IL-1β）］ were significantly upregulated in the model group （P<0.05， P<0.01）. Compared with the model group， the BBD-H group showed significantly decreased mRNA expression of HK1， HK2， PFKFB3， PFKFB4， PKM， LDHA， TNF-α， IL-6， and IL-1β （P<0.05， P<0.01）. Western blot results indicated that， compared with the normal group， the model group had significantly increased expression of glycolysis-related proteins ［glucose transporter 1 （GLUT1）， HK1， PFKFB3， and PKM］， inflammatory proteins ［interleukin-18 （IL-18）， TNF-α， and IL-1β］， and phosphorylated （p）-PI3K and p-Akt proteins （P<0.05， P<0.01）. Compared with the model group， the BBD-H group exhibited significantly decreased expression of GLUT1， HK1， PFKFB3， PKM， IL-18， TNF-α， IL-1β， p-PI3K， and p-Akt （P<0.05， P<0.01）. Metabolic indicator measurements showed that， compared with the model group， the BBD-H group showed significantly reduced GLU consumption， LD and ATP content （P<0.05， P<0.01）. ConclusionBBD may alleviate APAP-induced ALI through dual regulation of metabolic reprogramming and inflammatory responses， potentially via inhibition of the PI3K/Akt signaling pathway.

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.

With the extended survival period of breast cancer patients and the increasing health demands, the concomitant diseases of breast cancer have gradually attracted the attention of both doctors and patients, and it is imperative to conduct comprehensive management of these diseases, in which the general practitioners, as the more comprehensive and complex medical talents, have not yet played their due roles. In this article, we report two cases of comprehensive management of concomitant diseases of breast cancer through collaboration of general practitioners and specialists (integrated general and specialist care). The role and function of general practitioners in this process were deeply analyzed, and the establishment of a consultation-liaison general practice model to further promote the role of integrated general and specialist care in integrated oncology care was advocated.

Objective To investigate the effect of epifriedelanol(Epi)on gene expression of P-glycoprotein(P-gp)in human colorectal adenocarcinoma cell line LS174T and its mechanism.Methods LS174T cells were divided into control group and experimental-L,-M,-H groups.Experimental-L,-M,-H groups were treated with 5,10,20 μmol·L-1 Epi,respectively.Control group was treated with 0.1％dimethyl sulfoxide.Polymerase chain reaction was used to detect the mRNA expression level of P-gp.Theeffect of Epi on multidrug resistance protein 1(MDR1/P-gp)luciferase activity was investigated by pregnane X receptor(PXR)-MDR1/P-gp dual luciferase reporter gene assay.In addition,Western Blot was used to detect the protein expression level of P-gp and the nuclear factor-κB(NF-κB)pathway related proteins.Results The relative expression levels of P-gp mRNA in experimental-M,-H groups and control group were 52.24±5.19,23.00±3.52 and 100.00±9.00;the relative expression levels of P-gp protein were 86.37±9.96,74.85±15.92 and 100.00±12.91;the relative activities P-gp luciferase were 230.19±41.32,203.10±52.84 and 279.67±19.20;the relative expression levels of p65(RelA/p65)in nucleus were 132.36±23.93,145.96±25.15 and 100.00±10.88;the relative expression levels of phosphorylation NF-κB inhibits protein kinase α/β(p-IKKα/β)in cytoplasm were 184.00±54.82,290.10±49.59 and 100.00±15.34;the relative expression levels of phosphorylated NF-κB inhibitory protein α(p-IκBα)in cytoplasm were 125.73±18.77,133.69±20.25 and 100.00±8.12;the relative expression levels of IκBα in cytoplasm were 78.36±14.83,70.44±14.57 and 100.00±22.82,respectively.The above indexes of experimental-M and experimental-H groups were compared with control group,and the differences were statistically significant(P＜0.05,P＜0.01,P＜0.001).Conclusion Epi can down-regulate the gene expression of P-gp in human colorectal adenocarcinoma cell line LS174T,and the mechanism may be related to activation of NF-κB and suppression of PXR.

Immunometabolism studies focus on the relationships between immune cell functions and cellular energy metabolism pathways.Immunometabolism plays an important regulatory role in immune-related diseases.Mycobacterium tuberculosis(M.tb),an important intracellular pathogenic bacterium,enters alveolar macrophages after infection.The confrontation between M.tb and the host is a complex and dynamic process involving multiple aspects and mechanisms,such as the immune response,granuloma formation,and immune evasion.M.tb effector proteins play key roles in maintaining bacterial virulence and regulating host cell metabolism.This article reviews the reprogramming process of glucose metabolism,lipid metabolism,and immunometabolism,as well as changes in mi-tochondrial function in M.tb-infected host cells,thereby revealing the relationship between M.tb pathogenicity and host metabolic regu-lation,which is important for understanding tuberculosis.

This study was aimed at investigating the immunoregulatory function of Mycobacterium tuberculosis Rv3641c gene in modulating host type Ⅰ interferon responses.The shuttle plasmid pMV261 was used to construct Rv3641c overexpression recombinant Mycobacterium smegmatis,and the biological characteristics of the recombinant bacteria were analyzed to explore the effect of Rv3641c on the growth curve,colony morphology and stress resistance of Mycobacterium.Subsequently,RAW264.7 cells were infected with Rv3641c overexpressing Mycobacterium smegmatis,and the transcriptional expression of genes related to the inhibition of type I inter-feron pathway was determined by RT-PCR.The expression level of IFN-βprotein was determined by ELISA,and the intracellular sur-vival level was determined.As a result,the recombinant rMS::pMV261-Rv3641c was successfully constructed.The results of biologi-cal characteristics analysis showed that Rv3641c did not affect the growth of mycobacteria,but significantly changed the colony mor-phology of mycobacteria and improved its resistance to H2O2.The results of recombinant bacteria infection experiments showed that Rv3641c significantly down-regulated the transcription levels of IFN-α,IFN-βand downstream ISGs genes CXCL10,IFIT2 and IL-1β in host cells,and Rv3641c significantly down-regulated the transcription levels of IFN-α,IFN-βand downstream ISGs genes CXCL10,IFIT2 and IL-1βin host cells.The results of intracellular colonization experiments showed that the intracellular mycobacte-ria in the overexpression recombinant bacteria infection group were significantly higher than those in the empty vector group,indicat-ing that Rv3641c could promote the intracellular surviv al of mycobacteria.In summary,the Rv3641c gene of M.tuberculosis can inhibit the host type I interferon response and promote the intracellular survival of M.tuberculosis,which provides a new idea for further explor-ing the immune escape function of M.tuberculosis and the discovery of new targets for anti-tuberculosis drugs.

Chronic thromboembolic pulmonary hypertension(CTEPH)is a severe form of pulmonary hypertension(PH),and is classified as the fourth major category of pulmonary arterial hypertension.CTEPH is primarily caused by chronic thrombosis,leading to the obstruction of blood flow in the pulmonary arteries and result ing in a sustained increase in pulmonary artery pressure.The unclear pathogenesis of CTEPH,however,means that its early diagnosis is challenging,treatment options are limited,and prognosis assessment is often inaccurate.In-depth research into these mechanisms will thus improve our understanding of the pathophysiological processes of CTEPH,and also provide a theoretical basis for developing new therapeutic strategies.This review focuses on the current method of establishing CTEPH rat models and their advantages and disadvantages,offering researchers a reference for selecting and constructing CTEPH rat models.

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.