Charge density fluctuation determined the interlayer friction in bilayer MN4 (M = Be, Mg, and Pt).

MN4 (M = Be, Mg, and Pt) represents a new class of van der Waals materials. These materials are characterized by exceptional electrical and thermal conductivities, remarkable intralayer mechanical strength, and weak interlayer interactions, making them prone to shearing and slipping. Therefore, MN4 has significant potential applications as a solid lubricant. However, until now, there have been only limited comprehensive theoretical investigations focusing on the frictional properties of MN4 systems. Here, the frictional performances of MN4 are systematically analyzed by applying first-principles high-throughput calculations. The results reveal that interlayer friction of MN4 decreases from MgN4 to BeN4 and then to PtN4. The friction is directly determined by charge density variations during the sliding processes. The periodic formation and breaking of quasi-σ bonds in bilayer MgN4 leads to substantial variations in charge density and large interlayer friction. In contrast, the weak charge density alternations in PtN4 lead to rather low frictions in PtN4. Moreover, surface functionalization effectively diminishes friction within bilayer MgN4, but amplifies interlayer friction within bilayer PtN4, and under surface functionalization interlayer friction can be efficiently modulated by out-of-plane polarizations. Interestingly, HBr-MgN4 exhibits two orders of magnitude lower COF compared to intrinsic bilayer MgN4, leading to a phenomenon resembling superlubricity. These results significantly contribute to our understanding of the friction properties, offering valuable guidance for the practical implementation of MN4 in solid lubricants.

Mir-483 inhibits colon cancer cell proliferation and migration by targeting TRAF1.

MicroRNAs are important regulators during human growth and development. Emerging evidence indicates that microRNAs play important roles in colorectal cancer. The aim of this study is to reveal the biological function and direct target gene of miR-483 in colorectal cancer. The biological function of miR-483 on the proliferation and migration of colon cancer cells was then examined by Edu assay and transwell assay, respectively. Our findings revealed that miR-483 mimic could significantly inhibit cell proliferation and migration. The target gene of miR-483 was predicted by target scan software and identified by a dual fluorescence reporter system which showed that TRAF1 was a direct target gene of miR-483 in SW480 cell line. These data suggest that miR-483 is a colorectal cancer suppressor which could inhibit cell proliferation and migration, possibly via targeting TRAF1. The miR-483 could be a potential treatment target for colorectal cancer.

5-Azacytidine suppresses EC9706 cell proliferation and metastasis by upregulating the expression of SOX17 and CDH1.

5-Azacytidine is a well-known anticancer drug that is clinically used in the treatment of breast cancer, melanoma and colon cancer. It has been reported that 5-azacytidine suppresses the biological behavior of esophageal cancer cells. However, corresponding mechanisms remain unclear. In this study, using Transwell invasion and cell proliferation assays, we demonstrated that 5-azacytidine significantly inhibited the metastasis and proliferation of EC9706 cells, and upregulated the expression of cadherin 1 (CDH1) and SRY-box containing gene 17 (SOX17). Moreover, the inhibition of the metastasis of the 5-azacytidine-treated EC9706 cells was impaired following transfection with siRNA targeting CDH1 (CDH1 siRNA), and the inhibition of cell proliferation was attenuated following the downregulation of SOX17 by siRNA targeting SOX17 (SOX17 siRNA). Furthermore, 5-azacytidine remarkably reduced the CDH1 and SOX17 promoter methylation levels, suggesting that 5-azacytidine upregulates the expression of SOX17 and CDH1 by inhibiting the methylation of the SOX17 and CDH1 promoter. The findings of our study confirm that 5-azacytidine suppresses the proliferation and metastasis of EC9706 esophageal cancer cells by upregulating the expression of CDH1 and SOX17. The expression levels of CDH1 and SOX17 negatively correlate with the promoter methylation levels. CDH1 and SOX17 are potential indicators of the clinical application of 5-azacytidine.

Endoscopic stenting and concurrent chemoradiotherapy for advanced esophageal cancer: a case-control study.

AIM: To evaluate the role of endoscopic stenting with or without concurrent 3-dimensional conformal chemoradiotherapy (3D-CRT) in patients with inoperable esophageal cancer. METHODS: Advanced esophageal cancer patients indicated for esophagectomy received esophageal stents. A part of patients completed 3D-CRT after stenting. Efficacy was assessed by endoscopy and computed tomographic scan before and 4 wk after completion of the treatment. The median survival, 3D-CRT toxicity and complications were compared between 3D-CRT and control groups. RESULTS: From 1999 to 2008, 99 consecutive patients with T3/T4 disease and unsuitable for esophagectomy were placed with esophageal stents. Sixty-seven patients received 3D-CRT, while 36 patients treated with endoscopic stents alone were recruited as controls. After 3D-CRT treatment, the median tumor volume of 3D-CRT patients were reduced significantly from 43.7 ± 10.2 cm³ to 28.8 ± 8.5 cm³ (P < 0.05). The complete and partial response rate was 85.1%, and no response was 14.9%. After 3D-CRT, the incidence rate of T2 and T3 disease evident on CT scan increased to 78.4% while T4 decreased from 66.7% to 21.6% (P < 0.05). 3D-CRT Karnofsky Performance Status improved in 3D-CRT patients compared with the control group (P = 0.031). 3D-CRT patients had a longer survival than the control group (251.7 d vs 91.1 d, P < 0.05). And the median half-year survival rate in 3D-CRT group (91%) was higher than in the control group (50%, P < 0.05). The most common toxicity was leukocytopenia in the 3D-CRT group (46.7% vs 18.8%, P = 0.008). The control group had a higher rate of restenosis than the 3D-CRT group (81.3% vs 9.0%, P < 0.05). The rate of nephrotoxicity was increased in 3D-CRT as compared with the control group (31.3% vs 15.6%, P < 0.05). CONCLUSION: 3D-CRT can improve dysphagia in patients with inoperable esophageal carcinoma. 3D-CRT combined with stenting results in better survival as compared with endoscopic stents used alone.

Expression and clinical significance of syndecan-1 mRNA and HPA-1 mRNA in colorectal cancer detected with real-time fluorescent quantitative polymerase chain reaction.

BACKGROUND AND OBJECTIVE: Invasion and metastasis are the most common causes of mortality for patients with colorectal neoplasms, and blocking invasion and metastasis in a timely fashion has become a hot research focus. We investigated the expression of the messenger RNA of Syndecan-1 and HPA-1 in colorectal cancer, and their correlation with invasion and metastasis. METHODS: Real-time fluorescent quantitative polymerase chain reaction (PCR) was used to detect the expression of Syndecan-1 and HPA-1 in specimens from 49 patients with colorectal cancer, 49 paired adjacent colorectal neoplasms (2 cm from the carcinoma), and 49 surgical margins of paired normal colorectal mucosa tissue (5 cm from the carcinoma), to analyze their correlation with clinicopathologic characteristics of colorectal neoplasm. RESULTS: The expression of HPA-1 mRNA was significantly higher in colorectal cancer (40.56 +/- 11.75) than that in the paired adjacent colorectal neoplasms (18.28 +/- 11.33) and normal colorectal mucosa tissue (10.80 +/- 10.20) (all P < 0.001). The expression of HPA-1 mRNA was significantly higher in paired adjacent colorectal neoplasms than that in normal colorectal mucosa (P < 0.05). The expression of Syndecan-1 mRNA was significantly higher in normal colorectal mucosa (61.21 +/- 12.96) than in the paired adjacent mucosa (14.35 +/- 11.06) or colorectal cancer (10.12 +/- 8.58) (all P < 0.001). The expression of Syndecan-1 mRNA was significantly higher in the paired adjacent mucosa than that in colorectal cancer (P < 0.05). The decreased expression of Syndecan-1 mRNA and the increased expression of HPA-1 were closely associated with the degree of differentiation, the depth of infiltration, lymph node metastasis, vessel metastasis, and TNM staging of colorectal cancer (all P < 0.05). Spearman rank correlation analysis demonstrated a significant correlation between Syndecan-1 and HPA-1(r = -0.405, P < 0.05). CONCLUSIONS: The expression of Syndecan-1 mRNA was significantly highest in normal colorectal mucosa and the expression of HPA-1 mRNA was significantly highest in colorectal cancer. At the same time, the decreased expression of Syndecan-1 mRNA and the increased expression of HPA-1 mRNA can promote the invasion and metastasis of colorectal cancer. The determination of Syndecan-1 and HPA-1 may be of value in the treatment as well as in the prognosis of patients with colorectal cancer.