Search

OBJECTIVE: MiR-466 has been reported to exert a tumor-suppressive role in several cancers, including colorectal cancer and osteosarcoma, but its clinical significance and functional mechanisms in breast cancer (BC) pathogenesis still remain elusive. PATIENTS AND METHODS: The expression of miR-466 was determined using reverse transcription quantitative PCR. The clinical significance of miR-466 in BC patients was assessed by Chi-square test, Kaplan-Meier method and Cox regression analyses. Functional experiments, including CCK-8 and transwell assays, were performed to analyze cell proliferation, migration and invasion ability. The association between miR-466 and proteasome subunit α7 (PSMA7) was confirmed by Luciferase reporter assay. RESULTS: Here, we first observed that the expression of miR-466 was significantly downregulated in BC tissues and cell lines. The decreased miR-466 expression was significantly associated with tumor size (p = 0.003), lymph node metastasis (p = 0.008), TNM stage (p = 0.032) and poor survival rate. In addition, miR-466 was identified as an independent prognostic factor for BC patients. We further found that the overexpression of miR-466 significantly inhibited cell proliferation, migration and invasion. Mechanistically, PSMA7 was a potential target gene of miR-466 and negatively regulated miR-466 in BC cells. Oncomine database and Kaplan-Meier overall survival analysis indicated that upregulation of PSMA7 was associated with poor prognosis of BC patients. The rescue experiments demonstrated that PSMA7 overexpression reversed the effects of miR-466 on cell proliferation, migration, invasion and EMT transcription factors (E-cadherin, N-cadherin, and vimentin). CONCLUSIONS: Collectively, these results suggest that the miR-466/PSMA7 axis might have potential as a therapeutic target for BC treatment. [ABSTRACT FROM AUTHOR]

SnO2 quantum dots (QDs) are potential materials for deep ultraviolet (DUV) light emitting devices. In this study, we report the temperature and excitation power-dependent exciton luminescence from SnO2 QDs. The exciton emission exhibits anomalous blue shift, accompanied with band width reduction with increasing temperature and excitation power above 300K. The anomalous temperature dependences of the peak energy and band width are well interpreted by the strongly localized carrier thermal hopping process and Gaussian shape of band tails states, respectively. The localized wells and band tails at conduction minimum are considered to be induced by the surface oxygen defects and local potential fluctuation in SnO2 QDs. [ABSTRACT FROM AUTHOR]

Summary: What is known and Objective: The primary objective of this study was to compare the pharmacokinetics of dexmedetomidine in patients with end‐stage renal failure and secondary hyperparathyroidism with those in normal individuals. Method: Fifteen patients with end‐stage renal failure and secondary hyperparathyroidism (Renal‐failure Group) and 8 patients with normal renal and parathyroid gland function (Control Group) received intravenous 0.6 μg/kg dexmedetomidine for 10 minutes before anaesthesia induction. Arterial blood samples for plasma dexmedetomidine concentration analysis were drawn at regular intervals after the infusion was stopped. The pharmacokinetics were analysed using a nonlinear mixed‐effect model with NONMEM software. The statistical significance of covariates was examined using the objective function (−2 log likelihood). In the forward inclusion and backward deletion, covariates (age, weight, sex, height, lean body mass [LBM], body surface area [BSA], body mass index [BMI], plasma albumin and grouping factor [renal failure or not]) were tested for significant effects on pharmacokinetic parameters. The validity of our population model was also evaluated using bootstrap simulations. Results and discussion: The dexmedetomidine concentration‐time curves fitted best with the principles of a two‐compartmental pharmacokinetic model. No covariate of systemic clearance further improved the model. The final pharmacokinetic parameter values were as follows: V1 = 60.6 L, V2 = 222 L, Cl1 = 0.825 L/min and Cl2 = 4.48 L/min. There was no influence of age, weight, sex, height, LBM, BSA, BMI, plasma albumin and grouping factor (renal failure or not) on pharmacokinetic parameters. Although the plasma albumin concentrations (35.46 ± 4.13 vs 44.10 ± 1.12 mmol/L, respectively, P < .05) and dosage of propofol were significantly lower in the Renal‐failure Group than in the Control Group (81.68 ± 18.08 vs 63.07 ± 13.45 μg/kg/min, respectively, P < .05), there were no differences in the context‐sensitive half‐life and the revival time of anaesthesia between the 2 groups. What is new and conclusion: The pharmacokinetics of dexmedetomidine were best described by a two‐compartment model in our study. The pharmacokinetic parameters of dexmedetomidine in patients with end‐stage renal failure and hyperparathyroidism were similar to those in patients with normal renal function. Further studies of dexmedetomidine pharmacokinetics are recommended to optimize its clinical use. [ABSTRACT FROM AUTHOR]

The correlations of murine double minute 2 ( MDM2) T309 G and esophageal cancer were elucidated because the association between MDM2 expression states and clinicopathological parameters of esophageal squamous cell carcinoma ( ESCC) is controversial. We conducted a meta-analysis on studies screened from Pub Med, Web of Science, Embase, the Cochrane Library, and the Chinese Biomedical Literature Databases that were published before October 2014. All studies describing the association between MDM2 and ESCC were traced. Meta-analysis was performed using the STATA software ( Stata Corp., College Station, TX, USA). A total of 9 studies with 707 cases and 324 controls were included. MDM2 expression was higher in ESCC than in normal esophageal epithelium (odds ratio [ OR] 10.38, 95% confidence interval [ CI] 6.42-16.78, P < 0.001). High MDM2 expression was associated with early primary tumor stage ( T1/ T2 vs. T3/ T4, OR 0.59, 95% CI 0.38-0.92, P = 0.018) and increased risk of regional lymph node metastasis ( N0 vs. N1, OR 1.66, 95% CI 1.03-2.67, P = 0.039). However, no relationship was observed between MDM2 expression and the risk of distant metastasis ( OR = 2.09, 95% CI 1.00-4.36, P = 0.050), and MDM2 was not significantly correlated with TP53 expression ( OR 1.22, 95% CI 0.53-2.77, P = 0.643). Our analysis suggests that MDM2 acts as a potent marker of early primary tumor stage but higher risk of regional lymph node metastasis in ESCC. However, because of the limited number of studies included, the result should be further clarified by well-designed prospective studies. [ABSTRACT FROM AUTHOR]

In this paper, a simple, one-step chemical synthesis of Au@poly(m-phenylenediamine) (PMPD) core-shell nanoparticles by direct dropping aqueous chloroauric acid aqueous solution tom-phenylenediamine aqueous solution was reported, which is a facile and green method. We further evaluate the use of the obtained Au@PMPD to modify glassy carbon electrode and for H2O2electrocatalytic biosensing. The results indicate that the aggregated small Au nanoparticles in the inner part of PMPD could be an ideal sensing platform for H2O2detection. [ABSTRACT FROM AUTHOR]

We present an improved crossover adjustment procedure to determine mean sea surface height using TOPEX, 35-day repeat phase ERS-1, Geosat, and 168-day repeat phase ERS-1 satellite altimeter data. The mean sea surface frame defined by the TOPEX data is imposed as certain constraints in our crossover adjustment procedure rather than held fixed as in some other procedures. The new procedure is discussed in detail. Equations are developed to incorporate the a priori information of Topex data as well as other satellite altimeter data. The numerical computation result shows that the rms crossover discrepancies are reduced by an order of 1 cm when the Topex data is not fixed. Furthermore, the computed mean sea surface is less noisy and more realistic than that computed by the traditional procedure. [ABSTRACT FROM AUTHOR]

Objective: To investigate the role of an inflammatory microenvironment induced by Porphyromonasgingivalis ( P. gingivalis ) in the occurrence of esophageal squamous cell carcinoma (ESCC) in mice. Methods: A total of 180 C57BL/6 mice were randomly divided into 6 groups, i.e. control group, P. gingivalis group, 4NQO group, 4NQO + P. gingivalis group, 4NQO + P. gingivalis + celecoxib group, and 4NQO + P. gingivalis + antibiotic cocktail (ABC, including metronidazole, neomycin, ampicillin, and vancomycin) group, with 30 mice in each group, using the random number table. All mice were normalized by treatment with ABC in drinking water for 2 weeks. In the following 2 weeks, the mice in the control group and the P. gingivalis group were given drinking water, while the other 4 groups were treated with 30 μg/ml 4NQO in the drinking water. In weeks 11-12, the mice in the P. gingivalis group, the 4NQO + P. gingivalis group, the 4NQO + P. gingivalis + celecoxib group, and the 4NQO + P. gingivalis + ABC group were subjected to ligation of the second molar in oral cavity followed by oral P. gingivalis infection thrice weekly for 24 weeks in weeks 11-34. In weeks 13-34, the mice in 4NQO + P. gingivalis +celecoxib group and 4NQO + P. gingivalis + ABC group were administered with celecoxib and ABC for 22 weeks, respectively. At the end of 34 weeks, gross and microscopic alterations were examined followed by RT-qPCR and immunohistochemistry to examine the expression profiles of inflammatory- and tumor-molecules in esophagi of mice. Results: At 34 weeks, 4NQO treatment alone did not affect the foci of papillary hyperproliferation, diseased area, and the thickness of the esophageal wall, but significantly enhanced the foci of hyperproliferation (median 1.00, P ＜0.05) and mild/moderate dysplasia (median 2.00, P ＜0.01). In addition, the expression levels of IL-6 [8.35(3.45,8.99)], IL-1β [6.90(2.01,9.72)], TNF-α [12.04(3.31,14.08)], c-myc [2.21(1.80,3.04)], pSTAT3, Ki-67, and pH2AX were higher than those in the control group. The pathological changes of the esophageal mucosa were significantly more overt in the 4NQO + P. gingivalis group in terms of the foci of papillary hyperproliferation (median 2.00), diseased area (median 2.51 mm 2 ), the thickness of the esophageal wall (median 172.52 μm), the foci of hyperproliferation (median 1.00, P ＜0.05), and mild/moderate dysplasia (median 1.00, P ＜0.01). In mice of the 4NQO + P. gingivalis group, the expression levels of IL-6 [12.27(5.35,22.08)], IL-1β [13.89(10.04,15.96)], TNF-α [19.56(6.07,20.36)], IFN-γ [11.37(8.23,20.07)], c-myc [2.62(1.51,4.25)], cyclin D1 [4.52(2.68,7.83)], nuclear pSTAT3, COX-2, Ki-67, and pH2AX were significantly increased compared with the mice in the control group. In mice of the 4NQO + P. gingivalis group, the diseased area, invasive malignant foci as well as pSTAT3 and pH2AX expression were significantly blunted by celecoxib. Treatment with ABC markedly reduced the papillary hyperproliferative foci, invasive malignant foci, and pSTAT3 expression but not pH2AX. Conclusions: P. gingivalis promotes the occurrence of esophageal squamous cell carcinoma in mice by inducing an inflammatory microenvironment primed with 4NQO induced DNA damage. Clearance of P. gingivalis with ABC or anti-inflammatory intervention holds promise for prevention of esophageal squamous cell malignant pathogenesis via blockage of IL-6/STAT3 signaling and amelioration of inflammation.

The article "MiR-466 as a poor prognostic predictor suppresses cell proliferation and EMT in breast cancer cells by targeting PSMA7, by Y. Xiao, S.-J. Zhang, X. Yan, C. Wu, Q.-W. Liu, H.-X. Dong, L.-J. Wang, Y. Hu, published in Eur Rev Med Pharmacol Sci 2021; 25 (18): 5625-5635-DOI: 10.26355/eurrev&#95;202109&#95;26782-PMID: 34604955" has been retracted by the authors as they state that some data cannot be repeated by further experiments. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/26782.

Objective: To explore the effect and mechanism of peroxiredoxin1 (PRDX1) in epithelial mesenchymal transformation (EMT) of gastric cancer cells. Methods: The expression of PRDX1 protein was detected by immunohistochemistry (IHC) in 70 paraffin specimens of cancer and normal mucosa adjacent to gastric cancer, and the relationship between PRDX1 protein and clinicopathological characteristics was analyzed. Then PRDX1-small interfering RNA (siRNA) was synthetized and transfected into human gastric cancer cell line AGS, and 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H tetrazolium bromide (MTT) assay was used to test cell proliferation. Transwell chamber assay was employed to test invasion of cells. Real-time quantitative polymerase chain reaction (RT-qPCR) and western blot were utilized to test the expressions of PRDX1, E-cadherin, N-cadherin, vimentin, and claudin-1. Results: The positive rate of PRDX1 protein expression in gastric cancer was 81.4%, higher than that in normal mucosa (27.1%, P <0.05). The expression of PRDX1 protein was related to invasive depth and lymph node metastasis of gastric cancer ( P <0.05). The expressions of PRDX1 mRNA and protein in AGS cells (2.216±0.445, 1.212±0.136), were higher than those in GES-1 cells (0.342±0.041, 0.328±0.038) ( P <0.05). When PRDX1-siRNA was transfected into AGS cells, the proliferation of AGS cells was significantly inhibited (all P <0.05). The invasion and migration rate of AGS cells in the transfection group [(112.00±17.98), (50.87±9.79)%] were significantly lower than those of the negative control group [(192.50±22.02), (83.03±8.67)%] and blank control group [(193.83±22.40), (82.40±7.21)%] (all P <0.05). The expressions of mRNA and protein of N-cadherin, vimentin and claudin-1 decreased, while the expression of E-cadherin increased when PRDX1-siRNA was transfected into AGS cells ( P <0.05). Conclusion: PRDX1 may promote the development of gastric cancer by regulating the EMT of gastric cancer cells.