mTOR (Phospho-Thr2446) ELISA Kit

N-6-methyladenosine (m(6)A) is one of the most common RNA modifications in eukaryotes involved in the regulation of post-transcriptional gene expression, as well as the occurrence and development of diseases related to environmental exposures. Adverse factors produced by environmental exposures, such as reactive oxygen species, inflammation, and cyclobutane pyrimidine dimers, mediate m(6)A modification, thereby regulating downstream gene and protein expression, and signaling pathways, such as FTO/m(6)A RNA/p53 axis, PI3K/AKT/mTOR pathway, and PARP/METTL3/m(6)A RNA/Pol kappa pathway. Moreover, an imbalance in m(6)A methylation levels directly mediates disease pathogenesis. To date, some studies have detailed the mechanisms underlying environmental exposure-mediated global changes in RNA m(6)A methylation. Based on our current understanding, we aimed to elaborate on the molecular mechanisms through which RNA m(6)A methylation regulates gene expression under environmental exposures. In this review, we outline the biogenesis and functions of RNA m(6)A modification. Furthermore, we focus on the effects of environmental exposures on m(6)A levels and highlight the relationships between environmental exposures (doses and time) and m(6)A levels. Although the molecular mechanisms regulating gene expression remains to be elucidated, m(6)A has potential applications as a disease biomarker. (C) 2020 Elsevier Ltd. All rights reserved.

Colorectal cancer is one type of cancer with high incidence rate and high mortality worldwide. Thus, developing new chemotherapeutic drugs is important. The Selaginella doederleinii Hieron ethyl acetate (SDEA) extract showed good anti-colon cancer effect in vitro and in vivo, but its mechanism is unclear. This study aimed to further reveal the anti-colon cancer effect of SDEA and its possible mechanism. The effects on cell viability, apoptosis, autophagy, and cell cycle in colorectal cells (HT29 and HCT116) were studied using MTT assay, fluorescence microscopy, transmission electron microscopy, and flow cytometry. The mechanisms were further studied using cell transfection, Western blot, and real-time quantitative polymerase chain reaction assay. The effect of xenotransplantation in vivo was observed using immunohistochemistry. Results showed that SDEA inhibited cell proliferation and induced cell morphological changes, cell cycle arrest, autophagy, and apoptosis. It also induced loss of mitochondrial membrane potential, increased the autophagic flux, raised the ratio of Bax/Bcl-2, activated caspases, and inhibited PI3K-Akt-mTOR signaling pathways. Furthermore, SDEA inhibited the growth of xenograft tumors in a dose-dependent manner. Immunohistochemistry analysis confirmed the alteration of autophagy- and apoptosis-related proteins and immunohistochemical microvascular density in xenografts, which were consistent with the results in vitro. Therefore, SDEA is important for developing candidate drugs against colorectal cancers.