Deletion of Nrf2 leads to hepatic insulin resistance via the activation of NF-κB in mice fed a high-fat diet.

Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. Insulin resistance (IR) is important in the development and progression of NAFLD. Nuclear erythroid 2‑related factor 2 (Nrf2) has previously been reported to be a novel regulator in NAFLD.

Curcumin upregulates Nrf2 nuclear translocation and protects rat hepatic stellate cells against oxidative stress.

The present study aimed to investigate the protective role of curcumin against oxidative stress in rat hepatic stellate cells (HSCs)-T6, and to determine the possible underlying mechanisms. HSC-T6 cells were divided into three groups: Negative control group, oxidant-treated group and curcumin-treated group. Flow cytometry and spectrophotometry were used to measure the production of reactive oxygen species (ROS), and the levels of malondialdehyde (MDA) and glutathione (GSH).

Nrf2 is a potential prognostic marker and promotes proliferation and invasion in human hepatocellular carcinoma.

Background: Nuclear factor E2-related factor 2 (Nrf2 or NFE2L2) is abundantly expressed in cancer cells and relates to proliferation, invasion, and chemoresistance. Our early observations also found that expression of Nrf2 was up-regulated in kinds of cancer including human hepatocellular carcinoma (HCC) cells. But there are limited reports about the expression, significance, function of Nrf2 in HCC.

Nuclear factor-kappa B1 is associated with gastric cancer in a Chinese population.

Activated nuclear factor-κB (NF-κB) is associated with the pathogenesis of numerous cancers, such as gastric cancer (GC). Genetic polymorphisms in the genomic region containing nuclear factor-κB1 (NFKB1) have a plausible role in modulating the risk of GC. To identify markers contributing to the genetic susceptibility to GC, we analyzed 15 single nucleotide polymorphisms (SNPs, rs28362491, rs3774932, rs1598856, rs230531, rs230530, rs230528, rs230521, rs230498, rs230539, rs1005819, rs3774956, rs4648055, rs3774964, rs4648068, and rs3774968) in the genomic region containing NFKB1.

[miR-520a regulates ErbB4 expression and suppresses proliferation and invasion of esophageal squamous cell carcinoma].

Objective: To investigate the role of miR-520a in regulation ErbB4 expression and the biological behavior of esophageal squamous cell carcinoma (ESCC).

Methods: The role of miR-520a in regulating the expression of ErbB4 was investigated by Western blotting and luciferase reporter assay system. The effect of miR-520a on the proliferation and invasion of ESCC cells was detected by MTT and Transwell invasion assay, respectively.

miR-302b is a potential molecular marker of esophageal squamous cell carcinoma and functions as a tumor suppressor by targeting ErbB4.

Background: ErbB4 expression has been noted in various tumors, but its regulatory mechanism in esophageal squamous cell carcinoma (ESCC) remains unclear. The aim of this study was to investigate whether miR-302b regulates the expression of ErbB4 at the post-transcriptional level and to determine its expression, significance, and function in ESCC.

Methods: We used real-time reverse transcriptase-polymerase chain reaction to quantify the expression of miR-302b in 50 ESCC tissues and analyzed its relationship with clinicopathological factors and survival.

Role of cancer-related inflammation in esophageal cancer.

Esophageal cancer (EC) is the ninth most common malignancy with a poor prognosis. It is clear that improvements need to be made to reveal the exact molecular mechanisms of EC. Cancer-related inflammation (CRI) recently has been proposed as a major physiological hallmark of malignancy and has important value in diagnosis, treatment, and prognosis.

Helicobacter pylori eradication with ecabet sodium, omeprazole, amoxicillin, and clarithromycin versus bismuth, omeprazole, amoxicillin, and clarithromycin quadruple therapy: a randomized, open-label, phase IV trial.

Background: Helicobacter pylori infection is a substantial public health problem and plays etiological role in the pathogenesis of many gastroduodenal disorders. The addition of ecabet sodium is proven to improve the efficacy of the standard triple therapy. Our aim was to assess the efficacy and safety of ecabet sodium-containing quadruple therapy versus 10-day bismuth-containing quadruple therapy for H.

Curcumin attenuates insulin resistance in hepatocytes by inducing Nrf2 nuclear translocation.

Background/aims: NF-E2-Related Factor-2 (Nrf2) is a transcription factor that plays a crucial role in the cellular protection against oxidative stress. Curcumin has been reported to induce Nrf2 nuclear translocation and upregulate the expression of numerous reactive oxygen species (ROS) detoxifying and antioxidant genes in hepatocytes. This study was designed to investigate whether curcumin-induced Nrf2 nuclear translocation could reduce ROS-mediated insulin resistance in cultured LO2 hepatocytes.

15-Hydroxyprostaglandin dehydrogenase is a tumor suppressor of human gastric cancer.

Cyclooxygenase-2 (COX-2), the key enzyme in prostaglandin synthesis, is often over-expressed in human gastric cancer. Recently, 15-hydroxyprostaglandin dehydrogenase [NAD+] (15-PGDH), the key enzyme in prostaglandin degradation, was found to be down-regulated in human gastric cancer tissues, but little is known about its role in gastric tumorigenesis. In this study, expression plasmids containing 15-PGDH siRNA were constructed and transfected into the gastric cancer cell line MKN45, which expresses endogenous 15-PGDH at a high level.