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BACKGROUND: Our objective is to evaluate the application values and effects of nanocarbon negative imaging technology in surgery for patients with the fifth stage of chronic kidney disease complicated with secondary hyperparathyroidism (SHPT). METHODS: Eighty-nine patients with SHPT in the fifth stage of chronic kidney disease admitted to the Department of Thyroid and Breast Surgery at the Affiliated Hospital of Nantong University between January 2018 and August 2020 were selected. All patients underwent total parathyroidectomy (tPTX) and were randomly divided into a group receiving nanocarbon (observation group; group A) and a control group (group B). Patients were followed up for 6 months after surgery and several observation indexes were compared and analyzed. RESULTS: Compared with the control group, the parathyroid glands in the observation group treated with nanocarbon were more clearly exposed, and better performances were seen in the operation time, blood loss, and recovery rate of bone pain (P

Ferroptosis is a kind of programmed cell death that is characterized by iron dependence. It differs from apoptosis, necrosis, autophagy, pyroptosis, and other types of cell death. Some studies have found that most of the genes involved in the regulation of ferroptosis or act as markers of ferroptosis are related to the poor prognosis of cancer patients.This study evaluated the expression, mutation, and copy number variation (CNV) of 60 previously reported ferroptosis genes in breast cancer samples from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Unsupervised clustering of breast cancer samples with ferroptosis genes was performed, followed by enrichment analysis with Gene Set Variation Analysis (GSVA), mutation display, and correlation analysis of clinical characteristics. Based on the analysis of differences among groups, the ferroptosis-related genes were identified, and the consistent clustering of breast cancer samples was performed. The characteristic genes were screened by stochastic forest algorithm and COX analysis, and a ferroptosis score (ferr.score) model was constructed to evaluate the prognosis of breast cancer patients.Copy number amplification and deletion of ferroptosis genes are common in breast cancer. Breast cancer patients grouped by ferroptosis gene clusters showed significant differences in survival, immune cell infiltration, and enriched Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathways. The ferroptosis-related differential genes were identified by comparison among clustering groups of ferroptosis gene. Characteristic genes were screened from these ferroptosis-related differential genes to construct the ferr.score model. The scoring model could accurately distinguish and predict the survival prognosis and immunotherapy efficacy in breast cancer patients.Ferroptosis plays an important role in the occurrence and development of tumors. According to the ferr.score model, the breast cancer samples can be divided into two groups with significantly different prognoses. These results provide novel insights and ideas for immunotherapy in breast cancer patients.

Triple-negative breast cancer (TNBC) refers to breast cancer without significant expression of estrogen receptor (ER), progesterone receptor (PR), or human epidermal growth factor receptor 2. We sought to identify the hub genes and find the potential progression mechanism of TNBC as well as immunotherapeutic targets. First, we screened the overlapped hub genes of Immune and Stromal, and the tumor mutation burden gene sets, as well as the The Cancer Genome Atlas (TCGA)-TNBC data set. Among these hub genes, we performed gene set enrichment analysis (GSEA) and gene set variation analysis analyses to recognize and evaluate the hub genes. Moreover, immune cell infiltration was evaluated by the CIBERSORT algorithm and single-sample GSEA. In addition, the expression and methylation of scavenger receptor class A member 5 (SCARA5) in TNBC were verified by quantitative PCR and methylation-specific PCR. Also, MTT and transwell assays were used to assess the biological function of SCARA5 in TNBC. SCARA5 and CMA1 were listed, and they mainly participated in cancer-related signaling pathways and immune-related signaling pathways. Interestingly, SCARA5 was closely associated with tumor purity and immune cell infiltration. Moreover, we found that SCARA5 was significantly downregulated and hypermethylation was in the promoter of SCARA5 in TNBC tissues. Our study showed the role of SCARA5 in proliferation and migration of TNBC, and suggested that SCARA5 can potentially serve as a candidate immunotherapy target for TNBC.

BACKGROUND: The core goal of this article is to find some meaningful risk factors that can affect the postoperative hypoparathyroidism of thyroid cancer, create an effective prediction model on this basis, and use it to selectively implement routine prophylactic calcium supplementation for patients after thyroid carcinoma surgery. METHODS: The clinicopathological characteristics of patients with papillary thyroid carcinoma (PTC) who underwent conventional bilateral total thyroidectomy (TT) + bilateral central lymph node dissection from January 2020 to August 2021 in the Affiliated Hospital of Nantong University were retrospectively analyzed. Firstly, this study analyzed the relationship between postoperative hypocalcemia and hypoparathyroidism. Then, we included many potential risk factors such as gender, age, body mass index (BMI), lateral lymph node dissection (LLND) and so on and also performed univariate and multivariate analysis of the independent risk factors for postoperative hypoparathyroidism in patients, and established a predictive scoring model. RESULTS: Among the 401 patients with PTC, 50.1% developed postoperative hypoparathyroidism. There was significant difference in serum calcium concentration between normal parathyroid group and hypoparathyroidism group after thyroid carcinoma surgery. BMI

To investigate the transport mechanism of isorhynchophylline (IRN) by using the specific inhibitors of organic cation transporters (OCTs) and organic anion transporting polypeptides (OATPs) and attempt illustrate the metabolic mechanism of IRN in the liver. All animals were randomly divided into three groups: control group (only inject IRN), RIF group (inject IRN and rifampicin), and ADR group (inject IRN and adrenalone). The control group was injected with IRN via the caudal vein. The RIF group was injected with rifampicin (RIF) by gavage, and after 1 h, IRN was injected into the caudal vein. Similarly, the ADR group received adrenalone by the caudal vein, and after 0.5 h, IRN was injected into the caudal vein. Thereafter, blood samples were obtained by the heart punctures at 90 min, 180 min, and 300 min following drug administration. Rats were sacrificed at 300 min after drug administration; then, the liver tissue was harvested. The level of IRN was measured by using high-performance liquid chromatography (HPLC), and the Kp values were calculated. After RIF administration (OATPs inhibitors), the Kp value of IRN was slightly decreased when compared with that of the control group. Meanwhile, the Kp value of IRN was dramatically reduced compared to that of the control group following ADR administration (OCTs inhibitors). The results suggested that OCTs have mainly participated in the hepatic uptake process of IRN.

Bo-Hao Zheng,1,2,* Zhi-Xian He,3,* Juan Zhang,4,* Jing-Jing Ma,5,* Hong-Wei Zhang,1,2 Wei Zhu,1,2 Zhi-Min Shao,6 Xiao-Jian Ni1,2 1Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, People’s Republic of China; 2Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, People’s Republic of China; 3Department of General Surgery, Affiliated Hospital of Nantong University, Nantong, 226001, People’s Republic of China; 4Liver Cancer Institute, Zhongshan Hospital, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Fudan University, Shanghai, 200032, People’s Republic of China; 5State Key Laboratory of Reproductive Medicine, Department of Breast Surgery, Nanjing Maternity and Child Health Care Hospital Affiliated to Nanjing Medical University, Nanjing, 210004, People’s Republic of China; 6Department of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Cancer Center and Cancer Institute, Fudan University, Shanghai, 200032, People’s Republic of China*These authors contributed equally to this workCorrespondence: Xiao-Jian NiDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, People’s Republic of ChinaTel/Fax +86-21-64041990Email ni.xiaojian@zs-hospital.sh.cnZhi-Min ShaoDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Cancer Center and Cancer Institute, Fudan University, Shanghai, 200032, People’s Republic of ChinaTel/Fax +86-21-64175590Email shaozhimingfd@163.comBackground: Triple-negative breast cancers (TNBC), comprising about 20% of breast cancers, have a poor prognosis. Currently, there is no effective target therapy for TNBC. LncRNA TUSC7 has been identified as a tumor suppressor in osteosarcoma and colorectal cancer. In this study, we investigated the clinical significance and the biological function of TUSC7 in breast cancer.Methods: We retrospectively evaluated the expression level and clinical significance of TUSC7 in 90 paired breast cancer tissues and normal tissues. The proliferation, migration, and invasion assays were performed to investigate the biological function of TUSC7 in breast cancer. Finally, microarray, a luciferase reporter assay, and quantitative real-time polymerase chain reaction (qPCR) were used to explore the potential underlying mechanism of tumor suppressor role of TUSC7.Results: Low TUSC7 expression was found to be an independent prognostic factor of poor overall survival (OS) in TNBC patients. Ectopic expression of TUSC7 inhibited tumor cell growth both in vitro and in vivo. TUSC7 overexpression significantly promoted the sensitivity of MDA-MB-468 cells to paclitaxel and carboplatin. In terms of the mechanism, TUSC7 might perform its biological function through binding with miR-1224-3P and regulating its expression level. Besides, genes in cell cycle pathways, such as BUB3 (budding uninhibited by benzimidazoles 3) and TGF-ß (targeting transforming growth factor β) pathways were downregulated, and genes involved in the MAPK (mitogen-activated protein kinase) (TGFBR2, transforming growth factor-beta receptor 2), PI3K-AKT (phosphoinositide 3-kinase- AKT serine/threonine kinase 1) and NF-κB (nuclear factor-kappa B subunit) pathways were upregulated in TUSC7 knockdown MDA-MB-231 cells.Conclusion: The low TUSC7 expression is an independent prognostic factor of poor OS of TNBC patients. TUSC7 might inhibit breast cancer cell growth and metastasis both in vitro and vivo through binding with miR-1224-3P and regulating MAPK, PI3K/AKT, and NF-κB signaling pathways.Keywords: TUSC7, long non-coding RNA, MiR-1224-3P, triple-negative breast cancer, prognosis

A rapid method for the determination of total arsenic in soil by gas chromatography after pyrolysis is proposed. Arsenic was isolated from the soil sample by pyrolysis and absorbed by the absorption liquid. Additionally, arsenic derivatives from the dimercaprol (BAL)–arsenic reaction were determined by gas chromatography. A pyrolysis system was evaluated for the isolation of micro amounts of arsenic from soil. The optimized parameters for the pyrolysis system are as follows: temperature of the tube furnace, 1000 °C; thermal decomposition time, 35 min; carrier gas flow rate, 0.1 L·min−1; concentration of sodium hydroxide (NaOH) in absorption liquid, 0.8 mol·L−1; volume of absorption liquid, 20 mL. The limit of detection (3σ, n = 20) for arsenic in soil was found to be 0.15 μg·g−1, as determined using this pyrolysis method. The results obtained using this method for the standard soil samples (GBW07425 and GBW07454) are consistent with the certified values of these 2 aforementioned standard samples. The method was successfully applied to determine the total arsenic in some actual soil samples.

Background: Gastrodin possesses low toxicity and a broad range of pharmacological activities and exhibits beneficial effects in neurological diseases. This study investigated the effects of gastrodin (GAS) on analgesic, anti-inflammatory, anxiolytic and inhibition of ferroptosis. Materials and Methods: The chronic inflammatory pain model of C57BL/6J mice was established by hindpaw injection of complete Freund’s adjuvant (CFA). After GAS treatment, Thermal hyperalgesia test, Mechanical allodynia test, Elevated plus-maze (EPMT) and Open-field test (OFT) were performed to assess the behavioral changes of pain and anxiety. mRNAs of FTHI, GPX4, HO-1 and PTGS2 were measured by RT-qPCR. Results: In CFA-injected C57BL/6 mice, we found that the mechanical and thermal pain threshold was increased with treatment of GAS. In EPMT, the number of entries in open arms and retention times of open arms were increased by GAS. In the OFT, the time spent in the central area was also increased. Furthermore, GAS enhanced mRNA expressions of FTHI, GPX4 and H0-1, as well as decreased the expression of PTGS2 in a dose-dependent manner. Conclusion: GAS is effective in the treatment of mice chronic inflammatory pain and anxiety-like behaviors. It maybe exhibit potential neuroprotective effects through inhibition of ferroptosis.

Background: The outbreak of the Coronavirus Disease-2019 (COVID-19) has threatened the public health of the world, and may eventually lead to acute respiratory impoverishment syndrome (ARDS). ARDS is a clinical syndrome caused by intrapulmonary or extrapulmonary reasons, which has complex pathogenesis and high mortality rate, it’s also one of the important factors in death from the 2019 novel coronavirus (2019-nCoV) epidemic. It has been reported that traditional Chinese medicine (TCM) can exert a good effect in the process of treatment. The present study aimed to observe the protective effects of TCM formula Qingfei Paidu Decoction (QFPD) on ARDS rats and explore the pharmacodynamic mechanism of the compound. Methods: 24 male rats were randomly divided into 4 groups (n=6), blank control group, model group, QFPD group (18.6g·kg-1·d-1) and dexamethasone group (2mg·kg-1·d-1). Blank control group rats were given saline, whereas other groups were injected with oleic acid (OA) and lipopolysaccharide (LPS) successively to establish ARDS model, and observed the behavioral performance of rats after model building. The morphological changes of lung tissue under optical microscope were observed; rat lung index (LI) and lung permeability index (LPI) were measured; blood PH, partial arterial oxygen pressure (PaO2, mmHg), partial arterial carbon dioxide pressure (PaCO2, mmHg), arterial oxygen saturation (SaO2) were measured by blood gas analyzer; the levels of tumor necrosis factor-α (TNF-α), interleukin (IL-1β, IL-6, IL-8, IL-10), thromboxane B2 (TXB2), 6-keto-prostaglandin F1α (6-keto-PGF1α), kerbs von lungren 6 antigen (KL-6), C-reactive protein (CRP), and the expression of superoxide dismutase (SOD) were measured via test kit.Results: Compared with the model group, the two treatment groups could improve the respiratory and lung injury in rats, and could restore the expression levels of thromboxane, various cytokines and protein to varying degrees.Conclusions: QFPD and dexamethasone have protective effects on ARDS rats induced by jointly injecting OA and LPS, and QFPD has the better effect in between. These may be related to reducing the expression levels of IL-1β, IL-6, IL-8, TNF-α, CRP, TXB2, KL-6, and increasing the contents of IL-10, 6Keto-PGF1a and SOD vitality in the body.

Triple-negative breast cancer (TNBC) refers to breast cancer without significant expression of estrogen receptor (ER), progesterone receptor (PR), or human epidermal growth factor receptor 2. We sought to identify the hub genes and find the potential progression mechanism of TNBC as well as immunotherapeutic targets. First, we screened the overlapped hub genes of Immune and Stromal, and the tumor mutation burden gene sets, as well as the The Cancer Genome Atlas (TCGA)-TNBC data set. Among these hub genes, we performed gene set enrichment analysis (GSEA) and gene set variation analysis analyses to recognize and evaluate the hub genes. Moreover, immune cell infiltration was evaluated by the CIBERSORT algorithm and single-sample GSEA. In addition, the expression and methylation of scavenger receptor class A member 5 (

Background: This study analyzed the clinical data and general information of breast cancer patients who were admitted by the Affiliated Hospital of Nantong University and underwent lumpectomy, followed by sentinel lymph node biopsy (SLNB) to investigate the effect of tumor location on the sentinel lymph node (SLN) detection rate, obtain a clear understanding of the SLNB procedure and further promote the use of this procedure in the local area. Methods: This study involved a total of 118 patients who were diagnosed with breast cancer and admitted by the Affiliated Hospital of Nantong University for lumpectomy and SLNB between July 2015 and June 2019. An analysis was conducted to explore the role of tumor location in the detection of SLNs. Results: Tumor location was associated with the success rate of post-lumpectomy SLNB. In the case of tumor location in the upper outer quadrant (UOQ) of the breast near the axilla, the SLN detection rate was relatively low. In contrast, when a tumor occurred in any of the other quadrants or the UOQ next to the areola, the tumor location had no significant impact on the SLN detection rate. SLNB indicated that 102 out of the 118 patients had SLNs, with the detection rate of 86.4%. Particularly, for patients whose tumors were located in the UOQ near their axillae, the SLN detection rate was 30% (3/10). As to tumor location in other quadrants or the UOQ next to the areola, the SLN detection rate was up to 90.8% (99/109). Conclusions: The performance of post-lumpectomy SLNB is associated with tumor location. SLNB is recommended when the tumor site lies in the upper inner/lower outer/lower inner quadrants (UIQ/LOQ/LIQ) of the breast or the UOQ next to the areola. If the SLNB result turns out to be negative, there is no need to perform axillary lymph node dissection (ALND). For tumor location in the UOQ of the breast, especially when it is near the axilla, SLNB is not a favorable option after lumpectomy. It is recommended that the patient receive a core needle biopsy (CNB) before SLNB.

BACKGROUND: Aberrant DNA methylation plays a crucial part in cancer progression through the silencing of gene expression. The purpose of this article was to investigate the DNA methylation-driven genes in breast invasive carcinoma (BRCA) by using integrated bioinformatics analysis and in vitro experiments. METHODS: The methylation and expression profile data of BRCA patients were downloaded from the TCGA database. Besides, the MethylMix algorithm was performed to distinguish differentially methylation-driven genes. Moreover, methylation-specific PCR was used to test the methylation-driven genes. RESULTS: A total of 218 differentially expressed methylation-driven genes were obtained. Then, four of these genes were applied to establish a prognostic risk model. Moreover, we found that hypermethylation was in the CpG islands of the promoter of COX7A1 gene in BRCA tissues. Furthermore, we found that COX7A1 was significantly down-regulated BRCA tissues and the COX7A1 expression level was markedly increased in BRCA cells after 5-Aza-dC treatment. CONCLUSIONS: Our study reveals that aberrant promoter hypermethylation is critical for COX7A1 gene silencing in BRCA and that COX7A1 emerge as a new biomarker and therapeutic target for BRCA.

The enzyme immobilization and catalytic properties of metal-oxide framework (MOF) derivatives can be complemented by the synergistic effects associated with the doping of heteroatoms. Herein, the MOF derivative Ni-doped Co/CoO/NC was prepared under nitrogen by pyrolysis of bimetallic Ni-Co-Zeolitic Imidazolate Framework (ZIF). The introduction of defect sites in the cobalt oxide structure by nickel and the strong metal electron synergistic effect improved the conductivity of prepared composite. Afterward, myoglobin (Mb) and acetylcholinesterase (AChE) were immobilized respectively on carbon paste electrode (CPE) modified by Ni-doped Co/CoO/NC and conductive film to construct electrochemical sensors. The electrochemical behavior of small molecules including hydrogen peroxide (H2O2), nitrite (NO2–) and organophosphate pesticides (OPs) was investigated via various electrochemical methods. Constructed H2O2 and NO2– sensors have good linearity in the range of 4 × 10−6-1.5 × 10−3 M and 8 × 10−7-1.05 × 10−3 M, 1.05 × 10−3-2.05 × 10−3 M with limits of detection of 1.5 × 10−6 M and 3.0 × 10−7 M, respectively. The linear range of the OPs sensors was 5.0 × 10−12-5.0 × 10−8 g.m−1 for methyl parathion and 1.0 × 10−13-1.0 × 10−10 g.mL−1 for paraoxon, respectively. And detection limits are 1.8 × 10−12 g.mL−1 (S/N = 3) for methyl parathion and 4.6 × 10−14 g.mL−1 for paraoxon. By extension, heteroatom-doped MOF derivatives offer potential new function as electrode modifier for biosensors.

NIMA Related Kinase 6 (Nek6) is a protein kinase involved in various cellular processes, including cell cycle regulation, apopotosis, senescence, telomere maintainance and chemoresistance. In the present study, we investigated the role of Nek6 in breast tumorigenesis and the prognostic merit of Nek6 expression in breast cancer. Immunohistochemistry and Western blot analyses was conducted to determine the expression profile of Nek6 in 133 breast cancer specimens. Nek6 was overexpressed in a majority of breast cancer specimens, compared with the adjacent non-tumorous tissues. Furthermore, we revealed that high expression of Nek6 was associated with histologic grade, tumor size and TNM stage in breast cancer. Liner regression analysis showed a significant association between the levels of Nek6 and Ki-67. Cox regression analysis indicated that Nek6 expression was an independent prognostic predictor for breast cancer. Moreover, intracellular level of Nek6 was remarkably increased following the release from serum starvation in MCF-7 cells. EdU incorporation assay indicated that depletion of Nek6 remarkably impaired the proliferation of MCF-7 cells. Finally, spheroid formation assay revealed that interference of Nek6 led to diminished oncospheroid-forming capacity of breast cancer cells. In conclusion, our results imply that Nek6 plays a facilitating role in breast cancer cell proliferation and may serve as a promising therapeutic target for breast cancer.

Background Cancer metastasis is the major reason for cancer related deaths, and the mechanism of cancer metastasis still unclear. RPLP1, a member of a group of proteins known as ribosomal proteins, is associated with tumorigenesis and primary cell immortalization and is involved in cellular transformation. However, the expression and potential function of RPLP1 in TNBC remain unclear. Methods The expression of RPLP1 in TNBC tissues and cell lines were detected with Real-Time PCR and western blotting. 81 cases of TNBC tissue samples and adjacent non-tumor tissue samples were tested by immunochemistry to determine the correlation between the RPLP1 expression and clinicopathological characteristics. In vitro, we determined the role and mechanistic pathways of RPLP1 in tumor metastasis in TNBC cell lines. Results In this study, we detected high levels of RPLP1 expression in TNBC samples and cell lines. RPLP1 is upregulated in triple-negative breast cancer (TNBC) tissues and cells, and high expression levels correlate with an increased risk of recurrence and metastasis. Furthermore, high RPLP1 expression was associated with a poor prognosis and was an independent prognostic marker for TNBC. In RPLP1-induced cancer metastasis, RPLP1 may increase cancer cell invasion, which is likely the result of its effect on the cancer cell epithelial-mesenchymal transition. Conclusions Altogether, our findings indicate RPLP1 is a poor prognostic potential biomarker and anti-metastasis candidate therapeutic target in triple-negative breast cancer.

Junfei Xu,1,2 Feiran Wang,2 Xi Wang,3 Zhixian He,2 Xinguo Zhu1 1Department of General Surgery, First Affiliated Hospital, Soochow University, Suzhou, People’s Republic of China; 2Department of General Surgery, Affiliated Hospital, Nantong University, Nantong, People’s Republic of China; 3Medical College of Nantong University, Nantong, People’s Republic of China Background/purpose: Given the emerging role of microRNA (miRNA) in cancer progression, we investigated the role and mechanism of miRNA-543 (miR-543) in gastric cancer (GC).Materials and methods: Real-time quantitative polymerase chain reaction was conducted to quantify the expression of miR-543. Luciferase reporter assay was used to confirm the association between speckle-type POZ protein (SPOP) and 3'-UTR. Moreover, the role of miR-543 and SPOP in GC was detected using transwell assays. In addition, we investigated the function of miR-543 in the epithelial–mesenchymal transition (EMT) progression.Results: miR-543 was upregulated in GC. We identified SPOP as a direct target of miR-543, revealing its expression to be inversely correlated with miR-543 expression in GC tissues. Moreover, restoration of SPOP could inhibit miR-543-induced GC cell migration and invasion, whereas downregulation of miR-543 inhibited cell migration and invasion, which was partly abrogated by SPOP knockdown. Furthermore, our data also showed that miR-543 induced EMT of GC cells.Conclusion: Our results demonstrated that miR-543 functions as a crucial oncogenic miRNA in GC. It exerts strong tumor-promoting effects through targeting SPOP in GC cell migration and invasion. Keywords: gastric cancer, miR-543, SPOP, EMT, invasion and migration

SYF2, a known cell cycle regulator, is reported to be involved in cell cycle arrest by interacting with cyclin-D-type binding protein 1. In the present study, we investigated the role of SYF2 in human breast cancer (BC) progression. SYF2 was highly upregulated in BC tissues and cell lines, as per Western blot and immunohistochemistry analysis. The SYF2 expression level had a significant correlation with the tumor grade and Ki-67 expression. In vitro starvation-refeeding experiment and SYF2-siRNA transfection assay demonstrated that SYF2 could promote proliferation of BC cells, while SYF2 knockdown resulted in cells cycle arrest at G1/S phase, reducing the cell growth rate of BC cells. These results indicated that SYF2 promotes human BC progression by accelerating the BC cells' proliferation. SYF2 could be a novel therapeutic target in human BC therapies.

MicroRNAs (miRNAs) are small non-coding RNAs involved in an array of biological processes, and their dysregulation is associated with tumor development and progression. One such miRNA, miR-219-5p, is abnormally expressed in patients with colorectal cancer (CRC). In the present study, reverse transcription-quantitative polymerase chain reaction was performed to measure miR-219-5p expression in cells from both CRC tumors, and surrounding healthy tissue. MTT and invasion assays were used to determine the role of miR-219-5p in regulating CRC cell proliferation and invasion, respectively. A luciferase assay was then performed to assess the binding of miR-219-5p to the CAPS gene that encodes calcyphosin protein. The present study confirmed that miR-219-5p expression is significantly downregulated in CRC tissue. miR-219-5p knockdown promoted the growth of HCT-8 cells and increased the expression of calcyphosin protein (CAPS). On the other hand, overexpressing miR-219-5p inhibited HCT-8 cell growth and invasion, and downregulated CAPS expression. In addition, CAPS was identified as the functional downstream target of miR-219-5p by directly targeting its 3′-untranslated region. Therefore, miR-219-5p may function as a tumor suppressor by decreasing CAPS expression, and subsequently inhibit tumor proliferation and invasion. These results indicate that novel therapeutic strategies that increase miR-219-5p expression may be developed to treat CRC.

The topographic effect has long been recognized as one of problems for quantitative remote sensing. The paper compares the correction results of OLI data based on C model, Cosine model, SCS model, Minnaert model and pixel-based Minnaert Correction Method. The visual inspection, statistical analysis and regression analysis of images were used to analyze the results before and after correction of image. The results show that the C model has a better correction effect. The Cosine model and SCS model were significantly overcorrected. However, C model, Minnaert model and slope-based Minnaert model weakened the influence of terrain. By comparative analysis, the C correction method was optimal model for OLI image.

// Sujie Ni 1, * , Hongwei Wang 1, 2, * , Xiaolin Zhu 3 , Chunhua Wan 4 , Junfei Xu 5 , Chen Lu 6 , Li Xiao 6 , Jiaqi He 2 , Chongyi Jiang 2 , Wei Wang 2 , Zhixian He 5 1 Department of Medical Oncology, Affiliated Hospital of Nantong University, Nantong University, Nantong 226001, China 2 Bilary and Pancreatic Center, Huadong Hospital of Fudan University, Fudan University, Shanghai 200040, China 3 Department of Gastroenterology, Affiliated Hospital of Nantong University, Nantong University, Nantong 226001, China 4 Department of Nutrition and Food Hygiene, School of Public Health, Nantong University, Nantong 226001, China 5 Department of General Surgery, Affiliated Hospital of Nantong University, Nantong University, Nantong 226001, China 6 Department of Pathology, Huadong Hospital of Fudan University, Fudan University, Shanghai 200040, China * These authors have contributed equally to this work Correspondence to: Zhixian He, email: hezhixian@ntu.edu.cn Wei Wang, email: hdwangwei@fudan.edu.cn Keywords: CBX7, pancreatic cancer, prognosis, tumor suppression, PTEN Received: April 23, 2016 Accepted: November 21, 2016 Published: December 20, 2016 ABSTRACT Chromobox protein homolog 7 (CBX7), one of the polycomb group (PcG) proteins, is a transcriptional repressor involved in the regulation of cell proliferation and senescence. In the present study, we showed that CBX7 negatively regulates the proliferation, viability, chemoresistance, and migration of pancreatic cancer cells. Overexpression of CBX7 significantly inhibited the proliferation of pancreatic cancer cells in vitro and in vivo . Depletion of CBX7 facilitated their growth. CBX7 also impaired the viability and chemoresistance of pancreatic cancer cells. Transwell assays showed that CBX7 reduces the migratory capacity of pancreatic cancer cells. Of note, CBX7 reduced PTEN/Akt signaling in pancreatic cancer cells by increasing PTEN transcription, suggesting involvement of PTEN/Akt pathway in the tumor suppressive activity of CBX7. In addition, immunohistochemical analysis the CBX7 and PTEN expression in 74 surgically resected pancreatic ductal adenocarcinoma (PDAC) specimens revealed that CBX7 expression is significantly downregulated in pancreatic ductal adenocarcinoma, compared to normal pancreatic tissues. Reduced expression of CBX7 and PTEN was associated with increased malignancy grade in pancreatic adenocarcinoma, whereas maintenance of CBX7 and PTEN expression showed a trend toward a longer survival. These findings suggest CBX7 is an important tumor suppressor that negatively modulates PTEN/Akt signaling during pancreatic tumorigenesis.

PAQR3 is a tumor suppressor in breast cancer and its expression regulation mechanism has not been well elucidated. In this study, we found that PAQR3 expression was downregulated in breast cancer tissues, and the downregulation of PAQR3 expression was found to be significantly associated with aberrant methylation of the gene promoter. Methylation‑specific PCR showed that hypermethylation of the PAQR3 gene was observed in 71.8% of the breast cancers, whereas it was found in only 28.2% of the corresponding non‑tumor tissues. Moreover, we found that the PAQR3 promoter methylation status was related to lymph node metastasis (P=0.01). In addition, overexpression of PAQR3 inhibited breast cancer cell invasion and growth. Furthermore, PAQR3 expression was restored in MCF‑7 cells after treatment with the demethylating agent, 5-aza-2'-deoxycytidine, and the effect of demethylation induced invasion and proliferation suppression of MCF‑7 cells. Collectively, our results suggested that the aberrant methylation of PAQR3 underlies its downregulation in breast cancer and our data indicated that epigenetic silencing of PAQR3 gene expression by promoter hypermethylation may play an important role in breast cancer.

// Tao Tao 1, 2 , Zhixian He 3 , Zhiming Shao 1 , Haojie Lu 1, 2, 4 1 Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, P.R. China 2 Department of Chemistry, Fudan University, Shanghai 200433, P.R. China 3 Department of General Surgery, Affiliated Hospital of Nantong University, Nantong 226001, P.R. China 4 Key Laboratory of Glycoconjugates Research Ministry of Public Health, Fudan University, Shanghai 200032, P.R. China Correspondence to: Haojie Lu, e-mail: luhaojie@fudan.edu.cn Keywords: triple negative breast cancer, metastasis, TAB3, O-glcNAcylation Received: October 08, 2015 Accepted: January 29, 2016 Published: March 18, 2016 ABSTRACT O-GlcNAcylation is a post-translational modification that regulates a broad range of nuclear and cytoplasmic proteins and is emerging as a key regulator of various biological processes. Although previous studies have shown that increased levels of global O-GlcNAcylation and O-GlcNActransferase are linked to the incidence of metastasis in triple negative breast cancer (TNBC) patients, the molecular basis behind this is not fully understood. In this study, we have determined that the TAK1 binding protein 3 (TAB3) was O-GlcNAcylated at Ser408 by OGT in the TNBC, which was required for its Thr404 phosphorylation, TAK1 activation and downstream nuclear factor kappa B (NF-κB) activation in TNBC. O-GlcNAcylation of TAB3 was induced by p38 MAPK and it in turn enhances the TAK1 mediated p38MAPK activation, which forms the positive feedback loop in TAB3mediated NF-κB activation. In TNBC, TAB3O-GlcNAcylationmediated cell migration and invasion by activating its downstream NF-κB. The expression of TAB3 O-GlcNAcylation increased in TNBC patients, and it was significantly correlated with poor prognoses of the patients. Our study provides insights into the mechanism of TAB3 regulating activity and suggests its important implications in TNBC metastasis.

PSMB4, proteasome subunit β4, is a member of the ubiquitin-proteasome family, and is elevated in a variety of malignancies. However, the expression level and related mechanism of PSMB4 in breast cancer remains unclear. Therefore, the present study investigated the expression level of PSMB4 in eight pairs of breast cancer and adjacent normal tissues. In addition, the relationship between the expression of PSMB4 and the clinical data of 92 breast cancer patients was discussed. First, it was found that PSMB4 expression was obviously upregulated in breast cancer tumor tissues and cell lines (MDA-MB-231 and MCF-7), and its level was significantly associated with tumor grade (P=0.005), tumor size (P=0.047), Ki-67 expression (P=0.040) and the poor prognosis of breast cancer. The present results demonstrated that PSMB4 could promote the proliferation of breast cancer cells, and was positively correlated with the expression of PCNA using an in vitro starvation-refeeding experiment. In addition, PSMB4‑siRNA transfection assay suggested that PSMB4 knockdown can decrease NF-κB activity and cell viability, and result in cell cycle arrest at the G1/S phase. These findings revealed that PSMB4 might facilitate breast cancer progression by promoting cell proliferation and viability. In summary, PSMB4 may be recognized as an efficacious prognostic marker and potential therapeutic target for breast cancer.

Breast cancer is the second leading cause of cancer‑associated mortality in women worldwide. Strong evidence has suggested that Ran, which is a small GTP binding protein involved in the transport of RNA and protein across the nucleus, may be a key cellular protein involved in the metastatic progression of cancer. The present study investigated Ran gene expression in breast cancer tissue samples obtained from 140 patients who had undergone surgical resection for breast cancer. Western blot analysis of Ran in breast cancer tissues and paired adjacent normal tissues showed that expression of Ran was significantly increased in breast cancer tissues. Immunohistochemistry analyses conducted on formalin‑fixed paraffin‑embedded breast cancer tissue sections revealed that Ran expression was associated with tumor histological grade, nerve invasion and metastasis, vascular metastasis and Ki‑67 expression (a marker of cell proliferation). Kaplan‑Meier survival analysis showed that increased Ran expression in patients with breast cancer was positively associated with a poor survival prognosis. Furthermore, in vitro experiments demonstrated that highly migratory MDA‑MB‑231 cancer cells treated with Ran‑si‑RNA (si‑Ran), which knocked down expression of Ran, exhibited decreased motility in trans‑well migration and wound healing assays. Cell cycle analysis of Ran knocked down MDA‑MB‑231 cells implicated Ran in cell cycle arrest and the inhibition of proliferation. Furthermore, a starvation and re‑feeding (CCK‑8) assay was performed, which indicated that Ran regulated breast cancer cell proliferation. Taken together, the results provide strong in vitro evidence of the involvement of Ran in the progression of breast cancer and suggest that it could have high potential as a therapeutic target and/or marker of disease.

Breast cancer (BC) is one of the most fatal diseases and poses critical health problems worldwide. However, its mechanisms remain unclear. Consequently, there is an urgency to investigate the mechanisms involved in BC initiation and progression and identify novel therapeutics for its prevention and treatment. In this study, we identified karyopherin β-1 (Kpnβ1) as a possible novel therapeutic target for BC. Western blotting was used to evaluate the expression of Kpnβ1 in four pairs of tumorous and adjacent non-tumorous tissues. The results revealed that the protein level of Kpnβ1 was higher in the cancer samples compared with those in the corresponding normal samples. Immunohistochemistry was performed on 140 BC cases and indicated that Kpnβ1 was significantly associated with clinical pathological variables. Kaplan-Meier curve revealed that high expression of Kpnβ1 was related to poor BC patient prognosis. A starvation and re-feeding assay was used to imitate the cell cycle using the SKBR-3 cell line, indicating that Kpnβ1 plays a critical role in cell proliferation. The Cell Counting Kit-8 assay revealed that SKBR-3 cells treated with Kpnβ1-siRNA (siKpnβ1) grew more slowly than the control cells, while flow cytometry revealed that low-Kpnβ1 expressing SKBR-3 cells exhibited increased BC cell apoptosis. Furthermore, the interaction between Kpnβ1 and Her2 was clearly observed by immunoprecipitation, indicating that Kpnβ1-knockdown abrogated nuclear transport of Her2. In summary, our findings revealed that Kpnβ1 is involved in the progression of BC and may be a useful therapeutic target.

Styrene–maleic anhydride copolymer (SMA) was used as a compatibilizer to improve the interfacial interaction between graphene sheets and polystyrene matrix. SMA mediated graphene sheets are closely encapsulated by a polymer layer and uniformly dispersed compared to the graphene sheets without SMA. The presence of SMA not only improves the melt modulus and its frequency-independence, but also results in an earlier transition from liquid-like to solid-like, indicating the formation of a percolated conducting network at a low content of graphene with the assistance of SMA. Accordingly, the different frequency dependences of electrical conductivity also lead to a much lower threshold of 0.17 vol.% for SMA modified nanocomposites compared to 0.52 vol.% for the unmodified counterparts, further confirming the earlier formation of a graphene network in the matrix. The improved rheological and electrical properties of the polystyrene nanocomposites are attributed to the homogeneous dispersion of the graphene sheets and the enhanced interfacial interaction between the graphene sheets and the polystyrene matrix.

Bi2WO6 nanoplates were hydrothermally prepared and characterized by scanning electron microscopy (SEM) and X-ray diffraction (XRD). The synthesized Bi2WO6 nanoplates were then used to fabricate modified carbon paste electrode (Bi2WO6–CPE) by a simple rubbing method. The result of electrochemical impedance spectroscopy indicated electron transfer resistance of the Bi2WO6–CPE was reduced vastly compared with CPE. In the meantime, cyclic voltammetry experiment demonstrated the Bi2WO6 nanoplates could accelerate the rate of electron transfer for the electrochemical reaction of diethylstilbestrol (DES) and bisphenol A (BPA) on the electrode. Moreover, the as-prepared electrode exhibited good selectivity toward simultaneous determination of DES and BPA with a rather low detection limit. By using differential pulse voltammetry (DPV) method, low detection limits of 15 nM (S/N = 3) and 20 nM (S/N = 3) for DES and BPA were obtained, with the linear calibration curves over the concentration range 50–2100 nM and 70–1300 nM, respectively. In addition, the proposed sensor was applied for the determination of analytes in spiked milk samples extracted from milk powder.

Background: Aberrant DNA methylation plays a crucial part in cancer progression through the silencing of gene expression. The purpose of this article was to investigate the DNA methylation-driven genes in breast invasive carcinoma (BRCA) by using integrated bioinformatics analysis and in vitro experiments. Methods: The methylation and expression profile data of BRCA patients were downloaded from the TCGA database. Besides, the MethylMix algorithm was performed to distinguish differentially methylation-driven genes. Moreover, methylation-specific PCR was used to test the methylation-driven genes Results: A total of 218 differentially expressed methylation-driven genes were obtained. Then, four of these genes were applied to establish a prognostic risk model. Moreover, we found that hypermethylation was in the CpG islands of the promoter of COX7A1 gene in BRCA tissues. Furthermore, we found that COX7A1 was significantly down-regulated BRCA tissues and the COX7A1 expression level was markedly increased in BRCA cells after 5-Aza-dC treatment. Conclusions: Our study reveals that aberrant promoter hypermethylation is critical for COX7A1 gene silencing in BRCA and that COX7A1 emerge as a new biomarker and therapeutic target for BRCA.

Dyrk1B, also called minibrain-related kinase (Mirk), is a member of the dual-specificity tyrosine phosphorylation-regulated kinase (Dyrk)/minibrain family of dual-specificity protein kinases. It is a serine/threonine kinase involved in the regulation of tumor progression and cell proliferation. In this study, the role of Dyrk1B in breast cancer development was investigated. The expression of Dyrk1B was detected by Western blot and immunohistochemistry staining, both of which demonstrated that Dyrk1B was overexpressed in breast cancer tissues and cells. Statistical analysis showed that the extent of Dyrk1B expression was associated with multiple clinicopathologic factors, including tumor size, grade, estrogen receptor status, and Ki-67 expression, and that high expression predicted a poor prognosis. The growth of breast cancer cells was inhibited significantly after knockout of DYRK1B by small interfering RNA (siRNA). Moreover, FoxO1 could be phosphorylated by Dyrk1B, and then FoxO1 was shuttled from the cell nucleus into the cytoplasm, which might be the mechanism of Dyrk1B-mediated survival in breast cancer cells. The results suggest that Dyrk1B plays a key role in the progression of breast cancer and provides a new target for breast cancer therapy.

Various mechanical behaviors will happen at the same time when an engine operates. Based on this concept, in this paper, a systematical analysis method is presented to analyze the multiple mechanical behaviors (tribology, dynamics, stiffness, and strength) of the crankshaft-bearing system in an engine. By this method, the analyses of the tribology of bearing, the dynamics of crankshaft-bearing system and the dynamic stress of crankshaft can be accomplished simultaneously. For example, the effect of the journal misalignment of crankshaft and the elastic deformation of bearing bush on the dynamics of crankshaft-bearing system, the tribological performances of main bearings and the dynamic stress of crankshaft are analyzed emphatically. The results show that the journal misalignment of crankshaft and the elastic deformation of bearing bush have remarkable effect on the tribological performances of main bearings and the dynamic stress of crankshaft, but have little effect on the dynamics of crankshaft-bearing system.

Background and Aims We undertook this study to investigate the influence of PIRH2 (p53-induced RING-H2) protein on the proliferation and cell cycle of breast cancer cell lines. Methods PIRH2 expression was detected by Western blot analysis, immunohistochemistry (IHC) and Kaplan–Meier curve analysis. Cell proliferation was assessed by cell counting kit-8 (CCK-8). Cell cycle control was analyzed by flow cytometry. Results PIRH2 was up-regulated in breast cancer tissues and cell lines and up-regulated PIRH2 was highly associated with tumor size, grade, ER, and Ki-67. Moreover, Kaplan–Meier curve showed that up-regulated PIRH2 was related to the poor overall survival of patients with breast carcinoma. When the expression of PIRH2 was inhibited by siRNA transfection, cell proliferation was reduced. In addition, the number of G0/G1 phase cells was increased, but G2/M cells were not affected significantly. Conclusion Decrease of PIRH2 expression in the breast cancer cell line MDA-MB-231 resulted in reduced tumor cell growth via the inhibition of cell proliferation and the interruption of cell cycle transition.