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Objective There is still no definitely therapeutic evidence of a beneficial effect of chemotherapy with radiotherapy for older patients with esophageal squamous cell carcinoma (ESCC). We aim to determine the influence of chemoradiotherapy (CRT) and radiotherapy (RT) alone in patients aged 65 years or older with locally advanced ESCC. Methods We retrospectively analyzed 581 ESCC patients who underwent CRT and RT alone. Univariate and multivariate Cox regression analysis was used to analyze the impact of clinical factors on long‐term overall survival (OS) and progression-free survival (PFS). Finally, we compared the toxicity rates of these patients. Results The median OS and PFS of the overall population were 23.2 months (2.0–162.6 months) and 18.6 months (1.1–159.6 months). Multivariate Cox regression analysis showed that chemotherapy (p p p p = 0.015). The results also revealed that the CRT group has better OS and PFS than RT alone group for patients aged 65–74 years (both p p > 0.05). Besides, higher staged ESCC has the inferior OS and PFS than lower staged ESCC for patients received RT alone and aged 65–74 years (both p p Conclusions The present study suggested that CRT for locally advanced ESCC in patients aged 65 years or older had a significant benefit over RT alone in terms of OS and PFS. However, for patients aged 75 years or older, there was no statistically significant difference between CRT and RT alone. CRT should be performed with special attention in patients aged 75 years or older.

Yahua Wu, Jiancheng Li Department of Radiation Oncology, Fujian Medical University Cancer Hospital, Fujian Cancer Hospital, Fuzhou, Fujian, 350014, People’s Republic of ChinaCorrespondence: Jiancheng LiDepartment of Radiation Oncology, Fujian Medical University Cancer Hospital, Fujian Cancer Hospital, Jin’an District, Fuzhou, Fujian, 350014, People’s Republic of ChinaTel +8613906900190Email jianchengli_jack@126.comPurpose: This study aimed to evaluate the relationship of the percentage decrease of maximal esophageal wall thickness with pathological complete response (pCR) and recurrence in esophageal squamous cell carcinoma (ESCC).Patients and Methods: A total of 146 ESCC patients treated with neoadjuvant chemoradiotherapy (NCRT) and surgery were included. The prognostic factors for overall survival (OS) and disease-free survival (DFS) were analyzed. The recurrence site, time, and frequency were included in the analysis. The percentage decrease of maximal esophageal wall thickness after NCRT was determined with the formula: [(pre-post)/pre] × 100.Results: Overall, only 42 patients achieved pCR. Multivariable logistic analyses showed that the percentage decrease of maximal esophageal wall thickness (HR: 2.504; 95% CI: 1.112– 5.638, P=0.027) was independently correlated with pCR. In multivariable Cox analyses, a ≤ 40% percentage decrease of maximal esophageal wall thickness was an independent adverse factor for both OS (HR: 1.907, 95% CI: 1.149– 3.165; P=0.012) and DFS (HR: 2.054, 95% CI: 1.288– 3.277; P=0.003). Compared with patients with a ≤ 40% percentage decrease, those with a > 40% percentage decrease had better 5-year OS (29.0% vs 60.1%, P< 0.05) and DFS (27.8% vs 54.4%, P< 0.05). Perineural invasion (PNI) was also an unfavorable factor for OS (HR: 2.138, 95% CI: 0.094– 4.178; P=0.026). Lymph vessel invasion (HR: 2.874, 95% CI: 1.574– 5.248; P=0.001) and PNI (HR: 2.050; 95% CI: 1.044– 4.023; P=0.037) were independent prognosticators for DFS. The rates of local and distant recurrence were also significantly difference between those with a percentage decrease of ≤ 40% and of > 40% (P< 0.05).Conclusion: The percentage decrease of maximal esophageal wall thickness is associated with pCR and recurrence in ESCC patients who undergo NCRT and surgery and can thus be used to independently predict prognosis.Keywords: neoadjuvant, esophageal squamous cell carcinoma, esophageal wall thickness, pathological complete response, recurrence

Objective: Cyclin-dependent kinase regulatory subunit 2 (CKS2) plays a vital role in regulation of the cell cycle and cancer progression. However, the role of CKS2 in lung adenocarcinoma (LUAD) remains unkonwn. Here, we examined the prognostic value and biological functions of CKS2 in LUAD by using omics data of 1,235 LUAD samples from TCGA, GEO, and our own cohort as well as data of in vitro experiments. Methods: Kaplan-Meier was conducted to evaluate the prognostic value of CKS2 expression. The association between CKS2 expression level and tumor immune infiltration was explored using the single-sample Gene Set Enrichment Analysis (ssGSEA) and TIMER database. Functional enrichment analyses were performed to annotate the biological functions of CKS2 in LUAD. Furthermore, a series of in vitro experiments and immunohistochemistry were performed for validation. Results: CKS2 overexpression was correlated with the advanced stage, TP53 status, PD-L1 expression, and DNA hypomethylation. Moreover, patients with LUAD and high CKS2 expression exhibited poor overall survival. Functional enrichment analysis indicated that CKS2 was involved in cell division, cell cycle, DNA replication. Experiments in vitro indicated that CKS2 knockdown decreased the invasion and proliferation of LUAD cells and facilitated their apoptosis. ssGSEA and TIMER analysis revealed a negative correlation between CKS2 expression and the immune cell infiltration. Conclusions: In summary, High CKS2 expression was associated with poor prognosis and low levels of infiltrating immune cells in LUAD as well as with malignant phenotypes. Therefore, CKS2 may be a promising prognostic biomarker and therapeutic target in LUAD.

A water-soluble polysaccharide from Chaenomeles lagenaria (CLWSP-1) was purified and structurally identified. Then, response surface methodology (RSM) was performed to optimize the hot water extraction (HWE) of CLWSP-1. In addition, the antibacterial activity of CLWSP-1 was also evaluated. The results indicated that the polysaccharide CLWSP-1 mainly contained galacturonic acid, arabinose, and galactose, and its molecular weight was 1.23 × 102 kDa. The optimal HWE for extraction of CLWSP-1 was a ratio of water to solid of 48.9 mL/g, temperature of 91 °C, and an extraction time of 114 min; an ethanol concentration of 81% and a 1.24% concentration of CLWSP-1 were achieved. Moreover, the obtained CLWSP-1 had strong antibacterial activity when exposed to Escherichia coli and Staphylococcus aureus, suggesting that CLWSP-1 may potentially contribute to the development of a natural preservative in the food industry.

Background: Lung cancer has become the leading cause of cancer-related deaths worldwide with a rising trend of incidence and mortality. Lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) account for the major numbers, which should be paid enough attention. Advanced glycation end products receptor (AGER) is a multi-ligand receptor that interacts with a wide range of ligands. Previous studies have shown that abnormal AGER expression is closely related to immune infiltration and tumorigenesis. Nevertheless, the AGER DNA methylation relationship between prognosis and infiltrating immune cells in LUAD and LUSC is still unclear. Results: Compared with the normal lung tissues, the expression level of AGER was significantly reduced in LUAD and LUSC. Low expression of AGER was markedly correlated with histology, stage, lymph node metastasis and Tumor protein 53 (TP53) mutation and could be used as a potential indicator of poor prognosis of LUAD and LUSC. Further analysis showed that copy number variation (CNV), mutation and DNA methylation involved in the low level of AGER. Additionally, we found that AGER DNA hypermethylation meant a worse prognosis in LUAD and LUSC. In addition, we also found that hypermethylated AGER was significantly correlated with tumor infiltrating lymphocytes. Conclusion: AGER may be a candidate for the prognostic biomarker of LUAD and LUSC related with tumor immune microenvironment.

Yiping Zhang, Yahua Wu, Xufeng Zhou, Benyi Yi, Lili Wang Department of Biochemistry and Molecular Biology, Basic Medical College of Jiujiang University, Jiujiang City, Jiangxi Province 332000, People’s Republic of ChinaCorrespondence: Yiping ZhangDepartment of Biochemistry and Molecular Biology, Basic Medical College of Jiujiang University, No. 320, Xunyang East Road, Xunyang District, Jiujiang City, Jiangxi Province 332000, People’s Republic of ChinaTel +86-13767275087Email zhangyiping109@163.comPurpose: This study aimed to investigate the regulatory roles of estrogen receptor beta (ERβ) on gastric cancer (GC) cells, and reveal the potential mechanisms relating to nuclear factor-kappa B (NF-κB) signaling.Methods: GC cell lines SGC7901 and MKN45 were transfected with pEGFP-C1-ERβ to overexpress ERβ, and treated with PMA (a NF-κB activator) to activate NF-κB signaling. The cell proliferation and migration, as well as the formation of vessel-like structures in human venous endothelial cells (HUVECs) were detected. The expression of ERβ, NF-κB p65, p-NF-κB p65, Ki67 (a proliferation marker), vascular endothelial growth factor A (VEGF-A) and matrix metalloproteinase 2 (MMP-2), the DNA binding activity of NF-κB p65, the content of VEGF-A, and the activity of MMP-2 were detected in SGC7901 and MKN45 cells.Results: The transfection of pEGFP-C1-ERβ significantly increased the expression of ERβ in SGC7901 and MKN45 cells (P < 0.05). Overexpression of ERβ in SGC7901 and MKN45 cells significantly decreased the cell activity, cell number in G2/M phase, cell migration, the expression of Ki67, VEGF-A and MMP-2, VEGF-A content, MMP-2 activity, as well as the number of vessel-like structures formed by HUVECs (P < 0.05). Overexpression of ERβ also significantly decreased the DNA binding activity and the expression of p-NF-κB p65 in SGC7901 and MKN45 cells (P < 0.05). The anti-tumor effect of ERβ overexpression on GC cells was reversed by the intervention of PMA (P < 0.05).Conclusion: Overexpression of ERβ inhibited the proliferation, migration, and angiogenesis of GC cells through inhibiting NF-κB signaling.Keywords: estrogen receptor beta, gastric cancer, nuclear factor-kappa B, angiogenesis, proliferation

Purpose This study aimed to explore the role of Estrogen Receptor-β (ERβ)-mediated Notch signaling pathway in the regulation of proliferation and apoptosis in liver cancer cells. Methods HepG2 cells (Pbi-EGFP-ER) were transfected with ERβ that mediated by liposome, and normal HepG2 cells (Blank) and empty plasmid-transfected HepG2 cells (Pbi-EGFP-C) were used as controls. Then, Huh7 cells were transfected with shERβ lentivirus to knock down ERβ expression. The Huh7 cells were divided into three groups including Blank, experimental group (shERβ) and negative group (shLuc). Then, qRT-PCR, Western blot, CCK-8 assay, cell scratch assay, Transwell assay, Annexin V-FITC and PI double staining were performed based on these groups. Finally, a mouse xenograft model was constructed to verify the regulation of ERβ on Notch signaling pathway in liver cancer. Results In HepG2 cells, the ERβ expression in Pbi-EGFP-E group was higher than that in Blank and Bi-EGFP-C group. Overexpression of ERβ inhibited HepG2 cell proliferation, migration, invasion and Ki67 protein expression, as well as promoted apoptosis, Bcl-2 and Bax expression. Overexpression of ERβ decreased Notch1, Notch2 and Hes1 expression. In Huh7 cells, the effect of low ERβ expression was contrary to that of high ERβ expression. The shERβ + DAPT group reversed the effect of shERβ on the volume and weight of transplanted tumors. Conclusion ERβ may inhibit the development of liver cancer and promote apoptosis via inhibiting the Notch pathway.

Purpose This study aimed to evaluate the specific roles of estrogen receptor β (ERβ) on the invasion and migration of osteosarcoma (OS) cells and explore the regulatory mechanisms relating with Wnt signaling pathway. Methods The expression of ERβ was detected in human OS tissues by quantitative real-time PCR and immunohistochemistry. U2-OS cells were transfected with siRNA-ERβ (si-ERβ) to downregulate ERβ and treated with FH535 to inhibit Wnt signaling. The migration and invasion ability was detected by scratch and transwell assay, respectively. The expression of β-catenin, MMP-7, and MMP-9 was detected by Western blot. Subcutaneous tumor-bearing model was established by injection of U2-OS cells into mice, and the tumor volumes were measured. Orthotopic transplantation model was established by transplantation of tumor tissues into the liver of mice, and the metastatic tumors were counted. Results ERβ was downregulated in human OS tissues and U2-OS cells. The transfection of si-ERβ significantly increased the scratch healing rate; the number of invasion cells; and the expression of β-catenin, MMP-7, and MMP-9 in U2-OS cells. The injection of si-ERβ-transfected U2-OS cells into mice significantly increased the subcutaneous tumor volume; the expression of β-catenin, MMP-7, and MMP-9; and the number of metastatic tumors in liver tissues. The promoting effects of si-ERβ on the invasion and migration of U2-OS cells were significantly reversed by FH535 in vitro and in vivo. Conclusion Silencing of ERβ promotes the invasion and migration of OS cells via activating Wnt signaling pathway.

ObjectiveRadiation esophagitis (RE) is common in patients treated with radiotherapy (RT) for locally advanced esophageal squamous cell carcinoma (ESCC). We aim to construct a nomogram predicting the severe RE (grade ≥2) in patients with ESCC receiving definitive chemoradiotherapy (dCRT).Materials and MethodsLogistic regression was performed to evaluate the risk factors in predicting RE. Nomogram was built based on the multivariate analysis result. The model was validated using the area under the receiver operating curve (ROC) curve (AUC), calibration curves, and decision curve analyses (DCA). Spearman correlation analysis was used to evaluate the correlation between inflammation indexes.ResultsA total of 547 patients with stage II–IVA ESCC treated with dCRT from the retrospective study were included. Two hundred and thirty-two of 547 patients (42.4%) developed grade ≥2 RE. Univariate analysis indicated that gender (p = 0.090), RT dose (p < 0.001), targeted therapy (p = 0.047), tumor thickness (p = 0.013), lymphocyte-monocyte ratio (LMR, p = 0.016), neutrophil-lymphocyte ratio (NLR, p < 0.001), and platelet-lymphocyte ratio (PLR, p < 0.001) were the significant factors for a higher incidence of RE. In multivariate analysis, RT dose [p < 0.001; odds ratio (OR), 4.680; 95% confidence interval (CI), 2.841–6.709], NLR (p < 0.001; OR, 0.384; 95% CI, 0.239–0.619), and PLR (p < 0.001; OR, 3.539; 95% CI: 2.226–5.626) were independently associated grade ≥2 RE and were involved in the nomogram. ROC curves showed the AUC of the nomogram was 0.714 (95% CI, 0.670–0.757), which was greater than each factor alone (RT dose: 0.615; NLR: 0.596; PLR: 0.590). Calibration curves showed good consistency between the actual observation and the predicted RE. DCA showed satisfactory positive net benefits of the nomogram among most threshold probabilities.ConclusionsThe study demonstrated that RT dose, NLR, and PLR were independent risk factors for grade ≥2 RE in patients with locally advanced ESCC receiving dCRT. A predictive model including all these factors was built and performed better than it based on each separately. Further validation in large patient populations is still warranted.

Background The optimal lymph nodes dissection (LND) for esophageal adenocarcinoma (EAC) patients who underwent neoadjuvant chemoradiotherapy (NCRT) is controversial. Methods Patients were selected from Surveillance Epidemiology and End Results database. Multivariable Cox analysis was used to identify predictors of overall survival (OS). Restricted Cubic Splines (RCS) was used to examine the relationship between the number of LND and OS. Result 2,019 patients with non-metastatic EAC underwent NCRT were stratified into three groups according to LND using X-tile software: group 1: 1–8, group 2: 9–14, group 3: ≥15. In Multivariable Cox Regression analysis, the death risk was reduced by 22% (P = 0.001), 43% (P

Backgroud: Immune checkpoint inhibitors (ICIs) have been considered as a standard therapy for non-small cell lung cancer (NSCLC). This study aimed to explore associations between peripheral blood biomarkers with survival and immune-related pneumonitis (IRP) in patients with stage III/IV NSCLC treated with ICIs, and establish a novel risk stratification to predict outcomes.Methods: This study enrolled 95 patients with stage III/IV NSCLC receiving ICIs. Univariate and multivariate cox regression analyses were used to determine prognostic factors affecting overall survival (OS) and progression-free survival (PFS). Logistic regression analysis was applied to explore the correlation between peripheral blood markers and IRP.Results: Multivariate Cox analysis revealed that pretreatment absolute lymphocyte count (ALC) (HR: 0.113, 95%CI: 0.113–0.863, P=0.025), and post-treatment systemic inflammation response index (SIRI) (HR: 4.199, 95%CI: 1.058–16.662, P=0.041) were independent prognostic factors for OS. Similarly, pretreatment ALC (HR: 0.333, 95%CI: 0.129–0.857, P=0.023) and post-treatment SIRI (HR: 3.160, 95%CI: 1.046–9.551, P=0.041) were also independent predictors of PFS. Based on these biomarkers, patients were classified into 3 categories: low-risk group: ALC >1.5 and SIRI ≤1.69 (n=28); medium-risk group: ALC >1.5 or SIRI ≤1.69 (n=35); high-risk group ALC ≤1.5 and SIRI >1.69 (n=32). The 1-year OS rate were 69.2%, 63.6%, 27.1%, respectively (P=0.001) and 1-year PFS rate were 51.8%, 44.8%, 21.1%, respectively (P=0.007). Furthermore, we found patients with post-treatment NLR >3 were associated with a significantly higher risk for occurring IRP than that NLR ≤3 (HR: 2.917, 95%CI: 1.037-8.206, P=0.043), and the time to IRP onset in post-treatment NLR>3 group was significantly shorter than that in NLR≤3 (P=0.018).Conclusions: Pretreatment ALC and post-treatment SIRI appeared to be biomarkers of outcome in stage III/IV NSCLC patients treated with ICIs. Furthermore, post-treatment NLR>3 was more likely to develop IRP.

Highlight • Neoadjuvant chemoradiation (NCRT) followed by surgery was regarded as the standard treatment of locally advanced esophageal cancer. However, studies have reported that almost 31%−50% of esophageal cancer patients still have local recurrence and or distant metastasis after NCRT and surgery. At present, there are few reports on the risk stratification of patients with esophageal carcinoma after NCRT and surgery. The valuable effect of adjuvant chemotherapy in esophageal squamous cell carcinoma (ESCC) patients underwent NCRT followed by surgery remains controversial. There is also no consensus that whether patients need adjuvant chemotherapy. Reasonable risk stratification is therefore required that helps postoperatively surveillance and classify patients suitable for adjuvant chemotherapy. There remains, however, no reliable forecasting system for ESCC patients after NCRT and surgery. Based on the current status, we carry out a noval risk stratification to predict survival, recurrence and classify patients at high risk that may benefit from adjuvant therapy according to clinicophological factors, Objective Nowadays, there were few studies reporting the risk stratification of patients with esophageal squamous cell carcinoma (ESCC) after neoadjuvant chemoradiation (NCRT) and surgery. We aimed to establish a simple risk stratification to help postoperative detection and adjuvant treatment. Methods We included 146 patients with locally advanced ESCC who received NCRT followed by esophagectomy. The impacts of clinicopathological factors on overall survival (OS) and disease-free survival (DFS) were analyzed. The recurrence site, time, and frequency were recorded as well. Results The median follow-up was 53 months. The pathological complete respond (pCR) group demonstrated better 5-year OS and DFS (78.6% and 77.0%) than the non-pCR group (44.8% and 35.2%, all P

Background Lung cancer is the most common malignant tumor. Identification of novel diagnostic and prognostic biomarkers for lung cancer is a key research imperative. The role of centromere protein K (CENPK) in cancer is an emerging research hotspot. However, the role of CENPK in the progression of lung adenocarcinoma (LAC) is not well characterized. Methods In this study, we identified CENPK as a potential new gene for lung cancer based on bioinformatics analysis. In addition, in vitro experiments were performed to verify the function of this gene. We investigated the expression of CENPK in LAC by analyses of datasets from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Differential expression analyses, gene ontology (GO) enrichment, Kyoto encyclopedia of genes and genomes (KEGG) analysis, and gene set enrichment analysis (GSEA) were conducted to evaluate the diagnostic and prognostic relevance of CENPK. Then, for evaluating the biological behavior and role of CENPK in lung cancer cells, we did a series of vitro experiments, such as immunohistochemistry analysis, Western blot analysis, CCK8 assay, transwell assay, flow cytometry, and wound healing assay. Results We demonstrated overexpression of CENPK in LAC; in addition, increased expression of CENPK was associated with clinical progression. Moreover, CENPK was found to be an independent risk factor in patients with LAC. Furthermore, we observed activation of CENPK-related signaling pathways in patients with LAC. Conclusions Our findings indicate a potential role of CENPK in promoting tumor proliferation, invasion, and metastasis. It may serve as a novel diagnostic and prognostic biomarker in patients with LAC.

The mathematical model is used to evaluate the classroom teaching quality of foreign teachers in Sino-foreign cooperative education projects under the new engineering perspective. Based on the analytic hierarchy process, the main factors affecting the quality of foreign teachers' classroom teaching and their weights were studied. On this basis, a fuzzy comprehensive evaluation model of classroom teaching quality was established. The actual case shows that the method can evaluate the classroom teaching quality of foreign teachers from the perspective of new engineering subjects, and had certain practicality.

Zhang Y, Wu Y, Zhou X, Yi B, Wang L. Onco TargetsTher. 2019;12:9153—9164. The Editor and Publisher of OncoTargets and Therapywish to retract the published article. We were notified of potential image manipulation in thepublished article. The issues relate to the alleged duplicationof images shown in Figures 3B, 4B and 5A. Despiterepeated attempts to contact the authors, they have notresponded to our queries within the required timeframe.The editor determined the findings of the study were nolonger valid and requested for the article to be retracted. This retraction relates to this paper &nbsp

Background This study aimed to evaluate the specific roles of Estrogen receptor β (ERβ) on the invasion and migration of osteosarcoma (OS) cells, and explore the regulatory mechanisms relating with Wnt signaling pathway. Methods The expression of ERβ was detected on human OS tissues by quantitative real-time PCR and immunohistochemistry. U2-OS cells were transfected with siRNA-ERβ (si-ERβ) to downrgulate ERβ, and treated with FH535 to inhibit Wnt signaling. The migration and invasion ability was detected by scratch and transwell assay, respectively. The expression of β-catenin, MMP-7 and MMP-9 was detected by Western blot. Subcutaneous tumor-bearing model was established by injection of U2-OS cells into mice, and the tumor volumes were measured. Orthotopic transplantation model was established by transplantation of tumor tissues into the liver of mice, and the metastatic tumors were counted. Results ERβ was downregulated in human OS tissues and U2-OS cells. The transfection of si-ERβ significantly increased the scratch healing rate, the number of invasion cells, and the expression of β-catenin, MMP-7 and MMP-9 in U2-OS cells. The injection of si-ERβ-transfected U2-OS cells into mice significantly increased the subcutaneous tumor volume, the expression of β-catenin, MMP-7 and MMP-9, and the number of metastatic tumors in liver tissues. The promoting effects of si-ERβ on the invasion and migration of U2-OS cells were significantly reversed by FH535 in vitro and vivo. Conclusions Silencing of ERβ promotes the invasion and migration of OS cells via activating Wnt signaling pathway.

This study aimed to explore the role of Estrogen Receptor-β (ERβ)-mediated Notch signaling pathway in the regulation of proliferation and apoptosis in liver cancer cells.HepG2 cells (Pbi-EGFP-ER) were transfected with ERβ that mediated by liposome, and normal HepG2 cells (Blank) and empty plasmid-transfected HepG2 cells (Pbi-EGFP-C) were used as controls. Then, Huh7 cells were transfected with shERβ lentivirus to knock down ERβ expression. The Huh7 cells were divided into three groups including Blank, experimental group (shERβ) and negative group (shLuc). Then, qRT-PCR, Western blot, CCK-8 assay, cell scratch assay, Transwell assay, Annexin V-FITC and PI double staining were performed based on these groups. Finally, a mouse xenograft model was constructed to verify the regulation of ERβ on Notch signaling pathway in liver cancer.In HepG2 cells, the ERβ expression in Pbi-EGFP-E group was higher than that in Blank and Bi-EGFP-C group. Overexpression of ERβ inhibited HepG2 cell proliferation, migration, invasion and Ki67 protein expression, as well as promoted apoptosis, Bcl-2 and Bax expression. Overexpression of ERβ decreased Notch1, Notch2 and Hes1 expression. In Huh7 cells, the effect of low ERβ expression was contrary to that of high ERβ expression. The shERβ + DAPT group reversed the effect of shERβ on the volume and weight of transplanted tumors.ERβ may inhibit the development of liver cancer and promote apoptosis via inhibiting the Notch pathway.

Objective: Chaenomeles lagenaria fermented milk beverage was will to raw milk fermented yogurt after adding concentrated C. lagenaria juice, stabilizer and organic acid, sugar, water allocation. The production technology of fermented beverage for C. lagenaria and its stability were studied, thus for C. lagenaria the production technology of fermented beverage used to provide reliable reference for industrial production. Methods: Through the experiment, optimized condition of the production process of milk beverage, and to make good C. lagenaria stability of fermented milk beverage were studied. Results: add the yogurt, 40% 0.5% concentrated C. lagenaria juice stabilizer for optimum process conditions. The optimum proportion of stabilizers for sodium carboxymethyl cellulose 0.15%, polysaccharide compounds 0.1%, xanthan gum 0.2%. Conclusion: Through data analysis that C. lagenaria fermented milk beverage production need reasonable ratio of concentrated C. lagenaria juice and yogurt combine to produce fermented milk quality and taste are good C. lagenaria.

The present study aimed to explore the potential anti-tumor effect of ERβ overexpression and investigate its related mechanism in osteosarcoma. Cell cycle and apoptosis rates were measured by flow cytometry. Cell proliferation and formation of autophagosome were assessed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay and dansylcadaverine (MDC) staining assay. Cell migration and invasion were detected by wound healing assay and transwell assay. Western blot analysis was designed to detect the protein expressions of surviving, Bax, LC-3 П, Beclin-1, ERβ, TβRⅠ, TβRⅡ, Smad2, Smad3 and Smad7. Real-Time fluorogenic PCR was designed to examine the mRNA expressions of surviving, Bax, ERβ, TβRⅠ, TβRII, Smad2, Smad3 and Smad7. The results showed that ERβ overexpression inhibited cell proliferation, migration and invasion, blocked cell cycle, and induced apoptosis and autophagy. Additionally, ERβ overexpression significantly inhibited the expression of surviving, TβRⅠ, TβRⅡ, Smad2 and Smad3. Meanwhile, the expressions of Bax, LC-3 П, Beclin-1 and Smad7 were dramatically upregulated by ERβ overexpression. In conclusion, ERβ overexpression could inhibit cell proliferation, migration and invasion, block cell cycle, and promote apoptosis and autophagy in OS by downregulating TNG-β signaling pathway.