Recently, ERK and its upstream kinase MEK1/2 have been shown to be present in the mitochondria and shuttle to the cytosol or nuclei (10). Given the mitochondrial localization of PHB in our studies, PHB could activate ERK in the mitochondria, leading selleck bio to downstream signaling beyond the organelle. Nrf2 signaling is considered a double-edged sword in regard to single-cell protection from oxidative and electrophilic stresses vs. cancer cell survival. It is thought that Nrf2 suppresses cancer initiation through elimination of ROS and protection of DNA from oxidative damage. Many potential therapeutic compounds, such as pterostilbene, resveratol, and peracetylated (?)-epigallocatechin-3-gallate, that possess anti-inflammatory, antioxidant, and/or anticarcinogenic properties induce Nrf2 as their mechanism of action (5, 6).

However, after initiation of cancer, dysregulation of the Nrf2/Keap1 pathway promotes tumorigenicity and chemoresistance through upregulation of detoxification pathways in cancer cells (48). The link between chronic inflammation and increased risk of cancer in multiple organs is well established. Patients with IBD are at an increased relative risk of developing colorectal cancer compared with the general public (11). A valid concern regarding PHB overexpression is the potential to increase tumorigenicity due to upregulation of detoxification pathways, rendering cells resistant to death. However, our recent study showed th
Colorectal cancer (CRC) is one of the most common tumour types in the world, with about 400 000 deaths annually [1,2].

In the United States, despite a slight decrease in its incidence and mortality during the past two decades, CRC remains the third most common cancer, affecting about 140 000 people and Drug_discovery accounting for 50 000 cancer-related deaths per year [3]. In China, where the incidence rate was initially low, due to the changes in lifestyle and nutritional habits, the CRC rate is increasing by 4.2% annually [4,5]. Carcinoembryonic antigen (CEA) is the most commonly used tumour marker for the diagnosis of CRC and evaluation of prognosis or recurrence after treatment. The guideline of National Comprehensive Cancer Network (NCCN) indicated that for T2 or greater lesions, a CEA test is recommended at baseline and every 3 months for 2 years [6]. CEA can be detected and quantitatively measured in the serum and the tumour tissue of CRC patients, but their role in the prognosis of CRC remains controversial. The objective of this study was to compare the prognostic value of CEA both in tumour tissue and in serum of the patients with CRC.