RESUMO
To better understand the salt tolerance of the wild rice, Oryza coarctata, root tissue-specific untargeted comparative metabolomic profiling was performed against the salt-sensitive Oryza sativa. Under control, O. coarctata exhibited abundant levels of most metabolites, while salt caused their downregulation in contrast to metabolites in O. sativa. Under control conditions, itaconate, vanillic acid, threonic acid, eicosanoids, and a group of xanthin compounds were comparatively abundant in O. coarctata. Similarly, eight amino acids showed constitutive abundance in O. coarctata. In contrast, under control, glycerolipid abundances were lower in O. coarctata and salt stress further reduced their abundance. Most phospholipids also showed a distribution similar to the glycerolipids. Fatty acyls were however significantly induced in O. coarctata but organic acids were prominently induced in O. sativa. Changes in metabolite levels suggest that there was upregulation of the arachidonic acid metabolism in O. coarctata. In addition, the phenylpropanoid biosynthesis as well as cutin, suberin, and wax biosynthesis were also more enriched in O. coarctata, likely contributing to its anatomical traits responsible for salt tolerance. The comparative variation in the number of metabolites like gelsemine, allantoin, benzyl alcohol, specific phospholipids, and glycerolipids may play a role in maintaining the superior growth of O. coarctata in salt. Collectively, our results offer a comprehensive analysis of the metabolite profile in the roots of salt-tolerant O. coarctata and salt-sensitive O. sativa, which confirm potential targets for metabolic engineering to improve salt tolerance and resilience in commercial rice genotypes.
RESUMO
Abnormalities in the mitogen-activated protein kinase (MAPK) signaling pathway are a key contributor to the carcinogenesis process and have therefore been implicated in several aspects of tumorigenesis, including cell differentiation, proliferation, invasion, angiogenesis, apoptosis, and metastasis. This pathway offers multiple molecular targets that may be modulated for anticancer activity and is of great interest for several malignancies. Polyphenols from various dietary sources have been observed to interfere with certain aspects of this pathway and consequently play a substantial role in the development and progression of cancer by suppressing cell growth, inactivating carcinogens, blocking angiogenesis, causing cell death, and changing immunity. A good number of polyphenolic compounds have shown promising outcomes in numerous pieces of research and are currently being investigated clinically to treat cancer patients. The current study concentrates on the role of the MAPK pathway in the development and metastasis of cancer, with particular emphasis on dietary polyphenolic compounds that influence the different MAPK sub-pathways to obtain an anticancer effect. This study aims to convey an overview of the various aspects of the MAPK pathway in cancer development and invasion, as well as a review of the advances achieved in the development of polyphenols to modulate the MAPK signaling pathway for better treatment of cancer.
Assuntos
Proteínas Quinases Ativadas por Mitógeno , Neoplasias , Apoptose , Carcinogênese/metabolismo , Carcinógenos , Humanos , Sistema de Sinalização das MAP Quinases , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Neoplasias/tratamento farmacológico , Neovascularização Patológica , Polifenóis/farmacologia , Polifenóis/uso terapêutico , Transdução de Sinais , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismoRESUMO
Cancer accounted for almost ten million deaths worldwide in 2020. Metastasis, characterized by cancer cell invasion to other parts of the body, is the main cause of cancer morbidity and mortality. Therefore, understanding the molecular mechanisms of tumor formation and discovery of potential drug targets are of great importance. Gene editing techniques can be used to find novel drug targets and study molecular mechanisms. In this review, we describe how popular gene-editing methods such as CRISPR/Cas9, TALEN and ZFNs work, and, by comparing them, we demonstrate that CRISPR/Cas9 has superior efficiency and precision. We further provide an overview of the recent applications of CRISPR/Cas9 to cancer research, focusing on the most common cancers such as breast cancer, lung cancer, colorectal cancer, and prostate cancer. We describe how these applications will shape future research and treatment of cancer, and propose new ways to overcome current challenges.