(-) - Epicatechin regulates LOC107986454 by targeting the miR-143-3p/EZH2 axis to enhance the radiosensitivity of non-small cell lung cancer.

BACKGROUND AND OBJECTIVE: Non-small cell lung cancer (NSCLC) is a pernicious tumor with high incidence and mortality rates. The incidence rate of NSCLC increases with age and poses a serious danger to human health. The aim of this study was to determine the mechanism by which (-)-epicatechin (EC) alleviates NSCLC. METHODS: Twenty-four pairs of NSCLC tissues and cancer-adjacent tissues were collected, and A549 and H460 radiotherapy-resistant strains were generated by repeatedly irradiating A549 and H460 cells with dose-gradient X-rays. Radiotherapy-resistant H460 cells were successfully injected subcutaneously into the left dorsal side of nude mice at a dose of 1 × 105 to establish an NSCLC animal model. The levels of interrelated genes and proteins were detected by RT‒qPCR and Western blotting, and cell proliferation and apoptosis were evaluated by CCK‒8 assay, Transwell assay, flow cytometry, and TUNEL staining. RESULTS: LOC107986454 was highly expressed in NSCLC patients, while miR-143-3p was expressed at low levels and was negatively correlated with LOC107986454. Functionally, EC promoted autophagy and apoptosis induced by radiotherapy, restrained cell proliferation and migration, and ultimately enhanced the radiosensitivity of NSCLC cells. A downstream mechanistic study showed that EC facilitated miR-143-3p expression by inhibiting LOC107986454 and then restraining the expression of EZH2, which ultimately facilitated autophagy and apoptosis in cancer cells, inhibited proliferation and migration, and enhanced the radiosensitivity of NSCLC cells. CONCLUSION: EC can enhance the radiosensitivity of NSCLC cells by regulating the LOC107986454/miR-143-3p/EZH2 axis.

Numerical Investigation of Transient Breakdown Voltage Enhancement in SOI LDMOS by Using a Step P-Type Doping Buried Layer.

In this paper, the transient breakdown voltage (TrBV) of a silicon-on-insulator (SOI) laterally diffused metal-oxide-semiconductor (LDMOS) device was increased by introducing a step P-type doping buried layer (SPBL) below the buried oxide (BOX). Device simulation software MEDICI 0.13.2 was used to investigate the electrical characteristics of the new devices. When the device was turned off, the SPBL could enhance the reduced surface field (RESURF) effect and modulate the lateral electric field in the drift region to ensure that the surface electric field was evenly distributed, thus increasing the lateral breakdown voltage (BVlat). The enhancement of the RESURF effect while maintaining a high doping concentration in the drift region (Nd) in the SPBL SOI LDMOS resulted in a reduction in the substrate doping concentration (Psub) and an expansion of the substrate depletion layer. Therefore, the SPBL both improved the vertical breakdown voltage (BVver) and suppressed an increase in the specific on-resistance (Ron,sp). The results of simulations showed a 14.46% higher TrBV and a 46.25% lower Ron,sp for the SPBL SOI LDMOS compared to those of the SOI LDMOS. As the SPBL optimized the vertical electric field at the drain, the turn-off non-breakdown time (Tnonbv) of the SPBL SOI LDMOS was 65.64% longer than that of the SOI LDMOS. The SPBL SOI LDMOS also demonstrated that TrBV was 10% higher, Ron,sp was 37.74% lower, and Tnonbv was 10% longer than those of the double RESURF SOI LDMOS.

Silencing circPVT1 enhances radiosensitivity in non-small cell lung cancer by sponging microRNA-1208.

BACKGROUND: Radiotherapy is one of main useful therapies in non-small cell lung cancer (NSCLC). Nevertheless, the underlying mechanism between NSCLC cell radiosensitivity and effective treatment remains unclear. OBJECTIVE: The aim is to explore the relationship between circular (circ) RNA and NSCLC cell radiosensitivity. METHODS: CircRNA plasmacytoma variant translocation 1 (PVT1) and microRNA (miR)-1208 expression in NSCLC cells were assessed using quantitative reverse transcriptase PCR (qRT-PCR). NSCLC cells were transfected with si-PVT1 or miR-1208 inhibitor and then exposed to irradiation. Cellular biology behaviors were detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), Terminal deoxynucleotidyl transferase dUTP Nick-End Labeling (TUNEL), colony formation, invasion and western blot. Additionally, binding between circPVT1 and miR-1208 was testified by dual-luciferase reporter and RIP assay. RESULTS: CircPVT1 was upregulated in NSCLC cells after irradiation treatment. Silencing circPVT1 induced inhibition of NSCLC cell growth and invasion, accompanied by cell apoptosis and γ-H2AX expression. Moreover, NSCLC cell proliferation and invasion was further inhibited by irradiation treatment in circPVT1-silenced cells, indicating a strong radiosensitivity of NSCLC cells. CircPVT1 functions as a competing endogenous RNA of miR-1208. Silencing miR-1208 reversed NSCLC cell sensitivity response to irradiation and activated PI3K/AKT/mTOR pathway in circPVT1-silenced cells. CONCLUSIONS: Silencing circPVT1 enhanced radiosensitivity of NSCLC cells by sponging miR-1208.

Ectopic expression of RASSF2 and its prognostic role for gastric adenocarcinoma patients.

RASSF2 has recently been identified as a potential tumor suppressor that serves as a Ras effector in various types of human cancers. However, there have been few reports detailing this in gastric cancer. Samples of gastric adenocarcinoma from 276 Chinese patients with follow-up were analyzed for RASSF2 protein expression by immunohistochemistry. RASSF2 was expressed in up to 31.2% (86/276) of this group of gastric carcinoma. The expression of RASSF2 was significantly lower in carcinomas than in normal mucosas (P<0.05). RASSF2 corresponded positively with patient age, histological differentiation, depth of tumor invasion, regional lymph node and distant metastasis, and TNM stage (all P<0.05). Further multivariate analysis revealed that patient gender, depth of tumor invasion, distant metastasis, TNM stage and the expression of RASSF2 were independent prognostic factors for patients with gastric cancer. The Kaplan-Meier plot showed that the overall mean survival time of the patients with RASSF2-negative expression was shorter than that of patients with positive expression (χ(2)=156.874, P<0.0001). Moreover, RASSF2-negative expression had a much more significant effect on the survival of those patients with early stage tumors (χ(2)=127.167, P<0.0001), highlighted by a >50.9% reduction in 3-year survival compared to that of patients with RASSF2-positive expression. In late stages, the difference was also significant (χ(2)=6.246, P=0.019), with a 35.5% reduction in 3-year survival. It is suggested that RASSF2 plays an important role in the evolution of gastric adenocarcinoma and should be considered as a potential marker for its prognosis.